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Fukushima and Health: What to Expect 

Proceedings of the 3 r International Conference of the 
European Committee on Radiation Risk 

May 5 th /6 th 2009, 
Lesvos, Greece 

Edited by 

Chris Busby, Joseph Busby, Ditta Rietuma 

and Mireille de Messieres 



Brussels: European Committee on Radiation Risk 

Published in 201 1 by Green Audit 

Aberystwyth UK 



European Committee on Radiation Risk 
Comite Europeen sur le Risque de 1' Irradiation 

Secretary: Grattan Healy 

Scientific Secretary: Christopher Busby 

Website: www.euradcom.org 

Fukushima and Health: What to Expect 

Proceedings of the 2009 ECRR Conference on Radiation Risk, Lesvos, Greece 

Edited by: 

Christopher Busby, Joseph Busby, Ditta Rietuma and Mireille de Messieres 

Published for the ECRR by: 

Green Audit Press, Castle Cottage, Aberystwyth, SY23 1DZ, United Kingdom 

Copyright 201 1: The European Committee on Radiation Risk 

The European Committee on Radiation Risk encourages the publication of 
translations of this report. Permission for such translations and their publication will 
normally be given free of charge. No part of this publication may be reproduced, 
stored in a retrieval system, or transmitted in any form, or by any means, electronic, 
electrostatic, magnetic tape, mechanical, photocopying, recording or otherwise or 
republished in any form, without permission in writing from the copyright owner. 

The ECRR acknowledges support from and thanks: 

The International Foundation for Research on Radiation Risk, 

Stockholm, Sweden (www.ifrrr.org) 

The Department of Environment, University of the Aegean, 

Mytilene, Greece (http://www3.aegean.gr/) 



ISBN: 978-1897761-17-5 

A catalogue for this book is available from the British Library 



The ECRR acknowledges the assistance of the following individuals: 

Prof. Elena Burlakova, Russian Federation 

Dr Sebastian Pflugbeil, Germany 

Prof. Shoji Sawada, Japan 

Dr Cecilia Busby, UK 

Prof. Mikhail Malko, Belarus 

Prof. Angelina Nyagu, Ukraine 

Prof. Alexey Nesterenko, Belarus 

Dr Alfred Koerblein, Germany 

Prof. Roza Goncharova, Belarus 

Dr VT Padmanabhan, India 

Dr Joe Mangano, USA 

Prof. Carmel Mothershill, Canada 

Prof. Daniil Gluzman, Ukraine 

Prof. Hagen Scherb, Germany 

Prof. Yuri Bandashevsky, Belarus 

Dr Alecsandra Fucic, Croatia 

Prof. Michel Fernex, France/Switzerland 

Prof. Inge Schmitz Feuerhake, Germany 

Prof. Alexey V Yablokov, Russian Federation 

Prof. Christopher Busby, UK 

Prof. Vyvyan Howard, UK 

Mr Andreas Elsaesser, UK 

Mr Oliver Tickell, UK 

Mr Joseph Busby, UK 

Mm Mireille de Messieres, UK/France 

Ms Ditta Rietuma, Sweden/Latvia 

Mr Grattan Healy, Ireland 

Mr Richard Bramhall, UK 

Mr Joseph Busby, UK 

The agenda Committee of the ECRR comprises: 

Prof. Inge Schmizt Feuerhake (Chair), Prof. Alexey V Yablokov, Dr Sebastian 
Pfugbeil, Prof. Christopher Busby (Scientific Secretary), Mr Grattan Healy 
(Secretary) 

Contact: admin@euradcom.orR 




(from left) Inge Schmitz-Feuerhake, Hagen Scherb, Carmel Mothershill, Sebastian 
Pflugbeil, Alfred Koerblein, Guide, Shoji Sawada, Yuri Bandashevsky, Interpreter, 
Andreas Elsaessar 



ECRR 2009 Edward Radford Prize awarded 

by 

Mrs Jennifer Radford 

to 

Prof Yuri Bandashevsky 

Belarus 



Contents 

Editor's Foreword 1 

Credibility of the ICRP 2-5 

1. Prof. Christopher Busby. Radiation Risk: the present and the future; 
Requirements/or a comprehensive and accurate model 6-18 

2. Prof. Yuri Bandashevsky. Non cancer illnesses and conditions in areas 

of Belarus contaminated by radioactivity from the Chernobyl Accident 19-36 

3. Prof. Carmel Mothershill, Prof. Colin Seymour. Bystander effects 

and genomic instability Part 1: From the gene to the stream. 37-54 

4. Prof. Carmel Mothershill, Prof. Colin Seymour. Part 2: Human and 
Environmental Health Effects of low doses of radiation. 55-69 

5. Prof. Inge Schmitz-Feuerhake. How reliable are the dose estimates 

of UNSCEAR for populations contaminated by Chernobyl fallout? 70-85 

6. Prof. Roza Goncharova. Cancer risks of low dose ionising radiation 86-94 

7. Mr Andreas Elsaessar. Nanoparticles and Radiation 95-100 

8. Prof Sebastian Pflugbeil, Dr Alfred Koerblein. Childhood cancer 

near German nuclear power plants: The KiKK study 101-117 

9. Prof. Shoji Sawada. Estimation of Residual Radiation Effects on 
Survivors of the Hiroshima Atomic Bombing, from Incidence of the 

Acute Radiation Disease 1 1 8-143 

10. Prof. Mikhail Malko. Risk assessment of radiation-induced 

stomach cancer in the population of Belarus 144-184 

11. Prof. Mikhail Malko. Risk assessment of radiation-induced 

thyroid cancer in population of Belarus 185-196 

12. Prof. Daniil Gluzman. Tumours of hematopoietic and lymphoid 

tissues in Chernobyl clean-up workers 197-21 1 



13. Dr. Keith Baverstock. The ARCH Project and the health effects 

of the Chernobyl accident 212 

14. Prof. Hagen Scherb, Dr Kristina Voigt. Radiation induced genetic 

effects in Europe after the Chernobyl nuclear power plant catastrophe 213-232 

15. Prof. Angelina Nyagu. In Utero exposure to Chernobyl accident 

radiation and the health risk assessment 233-266 

16. Prof Alexey Yablokov. The real effects of the Chernobyl accident 

and their political implications 267-272 

17. Dr V T Padmanabhan. Sex ratio of offspring of A-bomb 

survivors -Evidence of Radiation-induced X-linked lethal mutations 273-293 

1 8 . Dr VT Padmanabhan. Underestimation of genetic and somatic 

effects of ionizing radiation among the A-bomb survivors 294-304 

19. Prof. Elena Burlakova. On the Assessment of Adverse 

Consequences of Chernobyl APS Accident on Health of 

Population and Liquidators 305-309 

19. Dr Alfred Koerblein, Prof N Omelyanets. Perinatal mortality 

in contaminated regions of Ukraine after the Chernobyl accident 3 1 0-3 1 7 



20. The Lesvos Declaration 3 1 8-322 



ECRR Proceedings Lesvos 2009 



Editor's Foreword 

First we should apologize for the length of time it has taken to produce the 
proceedings of this 3rd International Conference of the European Committee on 
Radiation Risk. I am writing this introduction in October 2011, some six months 
after the Fukushima catastrophe. The resolution of the dispute over the validity of 
the Radiation Risk model has never been more urgent. The ICRP risk model has 
been falsified by many studies, and now in addition, at the 2009 ECRR Lesvos 
conference, by the presentations collected here in these Proceedings. The stark 
revelations of illness following exposure to the fission products and uranium 
released by the Chernobyl accident are absolutely applicable to the illnesses which 
will develop inevitably in northern Japan following the Fukushima catastrophe. As 
Edmund Burke said "Those who don't know history are doomed to repeat it". The 
problem is that the nuclear industry and its powerful lobbies have so covered up the 
real effects of Chernobyl that no-one knows the real history of the effects of the 
widespread radioactive contamination. Many of these effects are to be found here. 
The Fukushima cover-ups are also the same: the same focus on external dose rates at 
the expense of internal exposures, the same talk about radiophobia, the same 
misleading (and absent) data, the same dreary sequence of nuclear industry 
spokespersons talking down the evidence, and bit by bit disappearing from the 
media slots as the true horror of the situation became apparent. 

What we have seen is the disappearance of the ICRP from Sweden 
following the resignation of its Scientific Secretary Jack Valentin. In this collection I 
have included a short exerpt from a videoed discussion I had with him just before 
the 2009 conference. The full video discussion is now available on the internet. It is 
clear that Valentin had decided to back off from the ICRP and its risk model. The 
ICRP has relocated to Canada with a new secretary, an individual with a MSc in 
Health Physics. But the writing has been on the wall for the ICRP for some time. 
The effects of Fukushima will act as a final proof of the total bankruptcy of its 
obsolete approach. There is no doubt about the health effects of the Fukushima 
catastrophe. All the Chernobyl effects presented here were caused by exposures to 
the same substances that now contaminate northern Japan. The cornerstone of 
Science Philosophy is the Canon of Agreement, which states that the antecedent 
conditions of a phenomenon, when repeated, will produce the same phenomenon. 
Let no one doubt that the Chernobyl experiment, repeated in Fukushima, will cause 
the same result, a result reported in these proceedings in all its terrifying clarity 
Chris Busby, 
Riga, September 201 1 



ECRR Proceedings Lesvos 2009 



The Credibility of the ICRP 

Partial transcript of conversation between Professor Chris Busby, Scientific 
Secretary of the European Committee on Radiation Risk, and Dr Jack 
Valentin, Scientific Secretary Emeritus International Commission on 
Radiological Protection. Part of a public meeting in Stockholm, 22 April 
2009 marking the 23rd anniversary of Chernobyl. 

CB: As scientists we ought to look at all sources of information, but ICRP has never 
cited any one of the many articles that falsify [ICRP] or which show your levels of 
risk are in error. Why? 

JV: This puts me in a slightly difficult position, of course, because I tend to agree 
with you — we should have quoted some of your stuff because since we don't agree 
with what you are saying we should then have said why we don't. [. . .] If you've got 
the Scientific Secretary of ICRP you press a button on its back and it says what it's 
supposed to say but I'm retired so I can say what I like. But not many people are 
greatly impressed by the evidence that you bring. It would have been much wiser in 
that situation to state more clearly why we are not impressed, thus giving you a 
chance to come back again. [Then we could have a debate and understand why we 
don't agree with each other.] 

CB: [cited as an example the 2006 ECRR publication Chernobyl 20 Years On and a 
"Russian studies" section of the 2004 Minority report of the UK Government 
Committee Examining Radiation Risks of Internal Emitters, CERRIE] . . . hundreds 
of references from the Russian language literature showing extraordinary effects 
from radioactivity - on genomic instability, genetic effects in plants and fish which 
cannot suffer from radiophobia — an enormous document which has been entirely 
ignored, suggesting bias. 

JV: I have already agreed [ICRP, UNSCEAR, BEIR should not ignore these 
findings] But we're not talking here about individual results but on most of them I 
believe my colleagues would make technical comments [on individual results]. 

CB: Don't the leukaemia clusters near nuclear sites falsify ICRP? 

JV: but there are other clusters around sites which were proposed for nuclear power 
stations but the reactors were not built. 



ECRR Proceedings Lesvos 2009 

CB: That study is confounded by the unused sites being on previously contaminated 
sea coasts and in areas of high rainfall [and high weapons fallout]. 

JV: We're now talking about confounders — that's the problem we have with all of 
your [epidemiological] studies. You have insufficient controls. ICRP has no official 
position on this but in principle people don't agree and will point to 
[epidemiological] studies where you get quite contradictory results, for example 
lowered cancer. Bernie Cohen and radon is the most famous, falsely showing a 
health benefit of radiation. 

CB: These arguments about confounding disappear in the case of infant leukaemia 
after Chernobyl. The babies were in the womb. The same results from 5 groups in 5 
countries published in different journals with doses calculated in microSieverts but 
statistically significant excesses. How do you explain that? 

JV: I can't, but I don't think you have enough explanations either. I honestly don't 
think you can convince me that you are right. There are technical arguments. We 
should have emailed reports and gone them slowly and thoroughly. That would be a 
clever way of continuing a discussion between ICRP and ECRR. 

CB: Yes and no, but to get here we have had to be robust, chaining ourselves to 
nuclear power stations, writing in the literature and using every possible method of 
publicising that your risk model is bankrupt. Otherwise we wouldn't be here. 

JV: Are you sure you wouldn't have had more success if you just came up friendly 
like and talked to the people at the Health Protection Agency? [UK radiation 
protection advisers] 

CB: [refers to long and well known experience of bad faith in various dialogues 
including by the Chairman and secretariat of CERRIE and the UK government 
departments involved.] 

JV: Yes and I have heard many stories not very favourable to you. It's a mistake to 
look back and argue about who did things wrong. Can't we look forward and be 
more constructive? 

CB: Yes, I agree. I have a question here that I was asked to put to you. It is "Can the 
ICRP model be used by Governments to predict the consequences of a nuclear 
accident, in terms of cancer yield?" 

JV: Basically no, because the uncertainties we are talking about would be too large; 
one order of magnitude. You are talking about two orders, but even at the one order 
I am talking about it's not useful for that sort of prognosis. 



ECRR Proceedings Lesvos 2009 

CB: What's the point of it then? 

JV: We're talking of the upper limit of course. Your most likely number of cases 
would be X but ten times X cannot be excluded. 

CB: Ok, ok, ok, and that means it is useful. So would the Government be formally 
reasonable, using ICRP risk models to calculate the risks — the cancer yield — 
from some hypothetical explosion at Barsebeck for example, even if they'd have to 
say it might possibly be ten times that predicted figure? Formally? 

JV: It would automatically be misused by both camps and that therefore is why it is 
not . . . you don't do it like that. You look at individual doses — the highest 
individual doses and calculate which is the sort of area where people should not live 
— which is the sort of area where they should have special needs — quick 
evacuation in case of emergency so this number exercise. I think it's just silly. It 
serves no good purpose whether you're in your camp or a pro-nuclear camp or an 
ICRP camp. 

CB: Well in this case I'm in a political camp [. . .] there are questions that politicians 
need to know the answer to. When you build new nuclear power stations, or 
[consider] any nuclear policy, you need to know what would happen if something 
went wrong. You need some kind of model, and at the moment they are using your 
ICRP model. Are you saying they should be or they shouldn't be? You seem to be 
saying they should use no model at all. Is it guesswork, or what? 

JV: Well I certainly wouldn't say they should use your model because . . . 

CB: ECRR gives the right answer 

JV: ... no it's the wrong answer, leading to large expenditure that would not be 
sensible and could be used to save lives in other [ways] 

CB: The draft ICRP Recommendations said that for many internal exposures the 
concept of absorbed dose was not valid. We would agree with that of course, but it 
disappeared from the final report. Why? 

JV: In fact there is a whole section of the Biological annex which talks about the 
difficulties. I don't know exactly why the specific statement disappeared but a 
person reading those paragraphs in the annex will be able to see there's huge 
uncertainty. 

CB: We're not talking about uncertainty but about the impossibility of using 
absorbed dose for internal nuclides. 



ECRR Proceedings Lesvos 2009 

JV: ICRP's position is that it's possible to use it albeit with large uncertainties. 

CB: How large is large? 

JV: Two orders is a very large uncertainty. 

CB: So it could be in error by two orders for some internal exposures — so we 
agree? 

JV: (laughing) I'd hate for you to go home and say "Jack agreed with me" 

CB: but I need an answer 

JV: Then the answer is I don't agree with you. (laughing) 

CB: but you just said Two orders of magnitude . . . 

JV: Yes but you can find, I'm sure you can find, an exceptional case, a specific case, 
where there would be that sort of uncertainty but remember it can go in another 
direction, and I'm sure that you can find in most cases there are uncertainties which 
are less than one order of magnitude, which you would find normally. If we look at 
the existing evidence I don't think you have enough evidence to prove your case. 

CB: The existing evidence is three orders of magnitude, if we take the childhood 
leukaemia clusters around nuclear sites; three orders. 

JV: That's what you are claiming on the basis of a handful of cases. 

CB: I'm claiming it on the basis of the German study, Aldermaston, Sellafield, 
Harwell and many others [...]# 

The full meeting was videotaped and can be seen on: 

www.youtube.com/watch?v=minY5smeLGKw 



Shortly after this meeting Busby addressed the Swedish radiation protection institute 
SRM. Deputy Director Carl Magnus Larsson said the ICRP model cannot be used to 
predict the health consequences of accidents. He added that for elements like 
Strontium and Uranium which bind to DNA national authorities would have the 
responsibility to assess the risks. Another SRM member said that the Secondary 
Photoelectron Effect was well recognised, also that in 1977 the ICRP had considered 
a weighting factor "n" for elements which bind to DNA but had not implemented it. 
Carl Magnus Larsson was sent to Australia where he still (Oct 201 1) is. 



ECRR Proceedings Lesvos 2009 
1 

Radiation Risk: the present and the future. 
Requirements for a comprehensive and accurate model 

Prof. Christopher Busby 

Scientific Secretary: European Committee on Radiation Risk ECRR 

UK Ministry of Defence Depleted Uranium Oversight Board (DUOB) 

UKDept of Health Committee Examining Radiation Risks from Internal Emitters 

(CERRIE) 

Leader: Science/ Policy interface; Policy Information Network for Child Health and 

the Environment (PINCHE; European Union). 

Guest Researcher: Julius Kuehn Institute, German Federal Agricultural 

Laboratories, Braunschweig 

Visiting Professor, Faculty of Life and Health Sciences, University of Ulster, 

Northern Ireland 



The ICRP radiation risk model, developed in 1952 and currently still the basis of 
legal limits has failed the human race and is now embarrassing in its manifest error. 
It is based on simple assumptions that in the great majority of cases fail to hold. 
Born in the statistical analysis of cancers in the Japanese A-Bomb victims, it firstly 
assumes that the risk of cancer is proportional to the absorbed dose or equivalent 
dose, in Joules per Kilogram - and that every cell within the organism receives the 
same ionisation, as the dose is simply divided by its mass. Secondly, it assumes a 
linear progression in risk (double the dose, double the risk of cancer) with no 
threshold, and thirdly it assumes that internal exposures can be accurately or 
sufficiently modelled as external exposures - that there exist no biochemical or local 
enhancements of the ionising effects of radiation at the scale of the target for 
radiation effects, the chromosomal DNA or other nanosized organelles. There are 
political and military dimensions which support the use of this model even when it is 
clearly incorrect - and these assumptions are manifestly incorrect. The 
epidemiology shows effects which occur at 'doses' which the model predicts are far 
too low to show any effect. 

Theory and Experiment 

External and internal isotope or particle doses confer hugely different ionisation 
density at the DNA level. Epithelial tissues and organelles concentrate certain 
isotopes due to biochemical or biophysical affinity. The resulting high levels of local 



ECRR Proceedings Lesvos 2009 

ionisation can make double strand breaks and so these effectswhich follow from this 
damage should be proportional to Dose squared. This is a simple kinetic theory 
argument since Second Event decays can intercept the repair mechanism, with 
obvious damaging effects. 

• DNA binding; membranes. Z4 (high Z elements uranium). 

• The dose response is not linear and can be biphasic. 

• No inclusion of ionisation density enhancement near DNA from Auger or 
transmutation. 

• Genomic and bystander effects mean non-cancer effects and possible field 
cancerization 

The epidemiological effects of low-dose ionisation are clear, but causality is denied 
on the basis of this false model. The effects of the Chernobyl disaster and the health 
following irradiation are clear in the ex-Soviet union and in children born across 
northern and western Europe. Cancer clusters, both adult and child exist around 
power plants, weapons laboratories and waste processing plants. 
Let me give some examples out of many. Many are listed in the ECRR2003 report 
and were discussed by the UK CERRIE committee but since then others have 
appeared which vindicate the model which we presented in ECRR2003. I list some 
of these in Table 1.1 below. 

Problems in the basis of radiation epidemiology 

Epidemiologists increasingly employ regression methods, and regression methods 
do not work if there is not a continuously increasing dose response. The result is that 
they give the answer that there is no association. Epidemiological results are 
routinely dismissed even by the epidemiologists on the basis that doses are too low 
to account for the effects, but Dose itself cannot be used for internal risk due to 
anisotropy. It has been noted that the dose response for many radiation studies, of 
health effects, in animals, in cell cultures and in biomarkers is often biphasic (Fig 
1.1). One example in the real world is the rate of infant leukemia in those exposed to 
the Chernobyl fallout [3]. In this cohort, which was extremely tightly described, the 
increases in leukemia were not a monotonic function of the estimated dose. The 
yield was largely biphasic, and very similar to that shown in Fig 1 . 1 There are two 
theoretical plausible reasons for such a response, both discussed in ECRR2003 [4]. 



ECRR Proceedings Lesvos 2009 

Table 1.1. Some examples of the development of cancer and other ill health in 
populations exposed to internal radionuclides which the current radiation risk model 
of the ICRP fails to predict or explain 



Example 


Effect 


Error factor 


Note 


Global 


Cancer epidemic, 


300-500 for 


Cancer increases easily seen 


atmospheric 


infant mortality, 


cancer 


in populations of Wales and 


tests 


heart disease 




England [1,3] 


Chernobyl 


Infant leukemia in 


400 


Published in two journals, 




Germany, Greece, 




discussed by CERRIE [2,3] 




Scotland, Wales, 




No other explanation 




Belarus 






Chernobyl 


Cancer in Sweden 


600 


Study by Tondel et al [6] 
shows increased cancer risk 
of 11% per surface 
contamination of lOOkBqm" 2 . 
Effect predicted by ECRR 
model [3] 


Chernobyl 


Global health 


Vary. Many 


Report by Yablokov et al in 




effects 


effects not 


New York Academy of 






predicted by 


sciences [4] 






current 








models 




Nuclear Test 


8-fold Child 


Not predicted 


Similar high congenital 


veterans 


congenital 


by current 


anomalies in Fallujah Iraq 




anomalies 


models 


due to Uranium weapons 
[9, 10] 


Uranium 


Very large 


1000 to 


Cancer in Gulf veteran now 


effects in Iraq 


increases in cancer 


10,000 


(2009) linked to DU 


Gulf veterans, 


and birth defects 




exposure by a coroner jury in 


Balkans 






UK [11] 


peacekeepers 








Childhood 


Sellafield and 


1000 to 


No other explanation 


cancer 


many others. Most 


10,000 




nuclear sites 


recent is KiKK 
study 






Irish Sea 


Sharp increase in 


1000 to 


Very high statistical 


coastal 


cancer risk near 


10,000 


significance. Inhalation of 


contamination 


coast 




particulates 



ECRR Proceedings Lesvos 2009 

But if the effect is a result of exposure to the fallout, we note that a regression 
approach would fail to find any statistically significant correlation. This is because 
the problem with regression is that it has to begin with an assumption of the 
relationship that is being tested, and the assumption is always that as the dose 
increases, the effect does also. But we know this isn't true for many relationships. 
Take the stretching of a wire as a result of increasing tension. We know that stress is 
proportional to strain only until the elastic limit and after that the wire breaks. This 
is also true for the fetus, exposed to radiation, and no doubt also to other systems. 
There only have to be two sensitivities of cells, or of individuals and a biphasic dose 
response results. The Youngs Modulus analogy in a living system would perhaps be 
the induction at lower doses of repair mechanisms and their overwhelming as the 
dose was increased. 

A second problem arises in retrospective epidemiology, the method of many 
studies of the effects of radiation exposure. It is now clear from, studies of 
Chernobyl exposed populations that exposure to radiation causes increased death 
rates from a wide range of causes, heart disease and strokes being among them. 
Since cancer is a disease mainly of old age, the competitive death rates from non 
cancer illnesses result in a reduction of the cancer rate in those populations exposed, 
since many die of other causes before they become old enough to develop cancer. I 
have found this recently in a re-examination of Thorotrast and Radium studies. In 
one Japanese study of Thorotrast exposed individuals there was a loss of almost 20 
years of lifespan in women compared with Japanese national deaths rates. This may 
be why these studies show only liver cancer effect in the very old. The destruction of 
bone marrow tissue and the likely resultant effects on health were drawn attention to 
by the head of the Medical Research Council, J F Loutit in 1970 and he specifically 
noted that these problems would affect the interpretation of the epidemiological 
studies of Radium Dial painters by Robley Evans and later researchers who 
employed retrospective analysis with cancer as an end point [7]. 

What we know and what we would like to know 

The Japanese A-Bomb studies are insecure because the control groups were exposed 
to internal radioactivity. For external exposures at least, the ICRP model cannot be 
too far in error: otherwise there would be large observed effects from medical 
exposures and from background radiation. Other external exposure studies do not 
show large differences except in the case of foetal exposures, and these are accepted. 
We do not know the effects of fractionation or multiple exposures occurring inside 
the cell repair timescale, and we do not know how the effects of repair system 
variation alter the epidemiological conclusions. 



ECRR Proceedings Lesvos 2009 



i run 



A 



mutated 



1% of cells are actively dividing 
and 200-600 times more 
radiosensitive than non-dividing 
cells 




DOSE 



Predicted dose -response relationship for mutation in animal 
with two types of cell sensitivity sub classes; high sensitivity 
replicating cells and low sensitivity quiescent cells. Sensitive sub-class 
are first mutated then killed as dose increases. 

Figure 1 - Predicted dose-response relationship for mutation Biphasic dose 
response: due to induced cell repair, sub classes of cell sensitivity, deaths of 
individuals, 

Although we do know the organ affinity (bone, prostate, muscle), we do not know 
the in vivo affinity of major radioactive elements for DNA; notably, uranium, 
barium, strontium, tritium, plutonium, radium. This is an extraordinary lack of 
knowledge in 2009. 

• We do not know the ionisation density at the DNA due to decays of various 
types and RBEs from internal elements located at different distances from 
the DNA. 

• We do not know the importance of membrane doses or the membrane 
affinity of major risk elements e.g. Cs-137. 

• We do not know what happens and what ionisations occur at the position of 
transmutation decay of an element bound to DNA e.g. Sr-90— Y-90. 

• We do not know the effects of multiple decays. 

• We do not know the local doses from Augers or Z4 elements bound to DNA. 

• We do not know the ionisation density near massive sub micron particles 
either radioactive or passive photoelectron amplifiers. 



10 



ECRR Proceedings Lesvos 2009 



Thankfully, both to the ICRP and others we do understand the bio kinetics of 
internal isotopes and tissue half-lives. We know the decay energies and mean 
absorbed doses to (large masses of) tissue, and the dose coefficients based upon 
these quantities. But it is not enough. 

The ICRP phantom 

For the ICRP and other current risk models the body is modelled as a bag of water, 
radiation is assumed external. Therefore, the ABSORBED DOSE is ENERGY 
divided by MASS, Joules/Kg = Gray. This method would give the same dose for 
warming yourself in front of a fire as eating a hot coal, and this is clearly 
problematic. 




lat 



Fig. 1 . Some irradiation geometries with an anthropomorphic phantom. 




ROT 



Figure 2 - Irradiation Geometries 



11 



ECRR Proceedings Lesvos 2009 







.'./fe-- J 



or ■ b 7? * 




'^j^t xy £■■■ 




Figure 3 - Alpha particle decays 
lung: 'Alpha Stars' 



Micron diameter particles of Plutonium in a rat 




INDIRECT EFFECT 
OH RADICAL 
FORMED! BOM 
IONIZATION OF 
WATER ATTA< k^ 
ONJ STRAND 



D1RJ t I EFFECT 
II KTRllNTRA- 
VI RSESONE 
STRAND 
(UNLIKELY) 

M PHA I RACKS 
HAVE HIGH DEN- 
SI ]Y(.»] IONIZA- 
TION AND IRA- 
VERSE BOTH 
STRANDS 

ISOTOPES* MIMI- 
CAL! Y ROUND TO 
DNA HAVK HIGH 

I MWCEOFCAUS- 
tNG noi ivi i 
STRAND BREAKS 



2 . c*^wsr& Prt^e 





1^)^ 






0*1 

J 1 



i-3i^ 



(MM 



Figure 4 - Some DNAP dimensions 

The internal doses to human populations from various processes have been 
calculated and are listed in the literature, e.g. UNSCEAR reports. One obvious way 
forward is therefore to employ weighting factors for the different internal exposures: 
this was the approach taken by ECRR2003. 



12 



ECRR Proceedings Lesvos 2009 










Sjw»6 ***** 



i^ b»*v^StoM$ 



Figure 5 - Cross Section ofDNAP with Uranyl ion on same scale 

We know from experiments with Auger emitters bound to DNA (e.g.I-125) that 
DNA is the target for the effects of ionising radiation (Fig 6). Therefore a rational 
way forward would be to attempt to calculate the ionisation density at the DNA for 
all radiation exposures. For high ionisation density we can employ second order 
kinetics and increase the risk accordingly. At minimum, even one such approach 
would put the current ERCC model on a more secure footing. 

It is an interesting thought experiment to consider the effects of the weak 
beta emitter Tritium. Tritium is afforded a RBE weighting factor of 1.0. But since 
the range of the beta emissions from Tritium are a few nanometres, it is clear that for 
uniform distribution of HTO in the body, in the cytoplasm, most of the beta energy 
cannot intercept the DNA and is effectively wasted. This means that the very small 
fraction of HTO that happened to be near the DNA is the cause of all the genotoxic 
effects. 



13 



ECRR Proceedings Lesvos 2009 










T£A<X ^5^ **tocn S(nS(HH £TtfwD> 



Fig 6 - Auger emitters 



Moving forward 

A secure radiation risk model must be based upon empirical data which compares 
similar exposures, and be able to explain all of these observations. It must be able to 
predict the outcome of specific exposures. It must not make unsupportable 
assumptions, and it must be able to employ historic exposure data to re-examine 
historical exposures and their effects. One avenue of progress is to develop the 
ECRR weighted risk factor approach to modelling internal exposures. At the same 
time, we must develop a way of comparing internal elements on the basis of their 
ionisation density at the DNA in order to support the semi-empirical approach. This 
is based upon the epidemiological results of internal exposures to mixed fission 
products which routinely give an error factor of 300 to 600 times for risk based on 
ICRP doses. This range, two to three orders of magnitude, explains all the 
observations of anomalous cancer yields following internal exposures to fission 
products and uranium. The Chernobyl accident exposures are a very valuable source 
of information, since they have isotope maps and in principle might yield health 
effects which can be tied to different isotopes. 



14 



ECRR Proceedings Lesvos 2009 

In general, exposure has been assessed in terms of Cs-137 as this can easily be 
measured, but in fact, Sr-90 is potentially a much more serious hazard. However for 
now, good news is around the corner. 

ICRP and Jack Valentin 

As many of you know, the mainstay of the ICRP is their Scientific Secretary, Dr 
Jack Valentin, from Sweden. Valentin is the editor of the latest version of the ICRP 
model [8] and has been involved in collating and publishing most of the ICRP works 
since the 1990s. He recently resigned from his position and was asked, just after 
this, by the Swedish anti nuclear organisation MILKAS to debate the issue of the 
two risk models, ECRR and ICRP in Stockholm. The meeting took place only a 
week or so ago, on 22 nd April (2009). The format was that we each gave an outline 
of our respective case and then there was a session where we asked each other 
questions. As a result of my questioning him, he made two extraordinary statements. 
Both were captured on video by Ditta Rietuma and have been put on the internet. 
The whole session was also recorded on digital media. These are the statements: 

1. The ICRP risk model cannot be used to predict the levels of cancer in 
populations exposed to ionising radiation. The reason is that there is too 
great an uncertainty about the risk coefficients for certain internal nuclide 
exposures. The uncertainties could be as high as two orders of magnitude. 

2. The ICRP and UNSCEAR were wrong to ignore the evidence from 
Chernobyl that their risk model was wrong and to ignore the evidence 
advanced by the ECRR that their risk model was wrong. 

When asked why he was saying these things now, Valentin said that when he was 
employed by ICRP he was unable to, but now he was no longer employed he was 
free to do so. 

I do not want you to imagine that Valentin is on our side, as it were. He made it 
quite clear that he did not agree with my position or that of the ECRR. What he did 
say is that the ICRP model was not safe for the purposes of analysing the outcome of 
exposures in the event of a nuclear accident, and that (inevitably) was incorrect 
when analysing the effects of the Chernobyl accident. 

Uranium effects and Court Cases 

It may be that the resignation of Jack Valentin has to do with some other recent 
developments in which I have been involved and which have had a significant 



15 



ECRR Proceedings Lesvos 2009 

impact on the acceptance of the ICRP model as a gold standard for radiation risk 
assessment. The first is the case of Uranium genotoxicity. As you know, Uranium, 
U-238, is considered a very low level hazard by ICRP. This is because its half life of 
some 4.5 billion years means that it has a very low specific activity, about 
12MBq/kg. The ICRP risk analysis provides the military with an excuse to employ 
uranium weapons for tank armour penetration and the uranium mining companies to 
avoid conceding that the many increases in ill health in those native Americans 
living on Uranium mine waste are a consequence of their exposures. Like most of 
the arguments in this area of radiation risk the absorbed doses are calculated and 
shown to be too low for the observed effects. 

However, there is one way in which Uranium exerts an influence on 
absorbed dose that has been entirely overlooked by the ICRP model. My PhD 
student at the University of Ulster, Andreas Elsaessar, will be addressing this later in 
the programme but I will say something here about it. I first pointed out in 2003 that 
since physics tells us that gamma radiation is absorbed by elements in proportion to 
the fourth power of their atomic number Z, internal contamination by high Z 
elements will attract natural background gamma radiation into the body. This 
radiation will be mostly converted to photoelectrons of almost the same energy as 
the gamma. Photoelectrons are, of course, identical to beta particles or any other 
energetic electrons that are produced in the body following gamma irradiation. If the 
Uranium contamination is relatively low, this would just increase the absorption of 
gamma rays, the absorbed dose, by a tiny fraction. But this is not all. It turns out that 
Uranium, as the U02++ ion has an enormously large affinity for DNA, binding to 
the phosphate backbone. The affinity constant is 10E+10 per mole. It follows that in 
the body, most of the soluble Uranium is bound to the DNA, including germ line 
DNA, mitochondrial DNA and chromosomal DNA. It follows that nanoparticle 
Uranium has a very high local absorbed dose due to photoelectrons. Its intrinsic 
radioactivity is not relevant here: this is a secondary photoelectron effect and would 
occur with other high Z particles like platinum and gold. Indeed, recently this effect 
has been employed to destroy tumours by injecting them with gold nanoparticles and 
then irradiating with X-rays. I have applied for a patent to use uranium in the same 
way, not nanoparticles but uranyl ion, which, I argue will stick to the tumour DNA 
at Urranium doses which are quite low and within the range found not to cause 
significant health effects in human populations. Of course, the effects of this 
discovery, are to demonstrate a plausible mechanism for the clear ill health effects 
manifested by Uranium in places like Iraq, and other battlefield areas, and also of 
course, in those who became contaminated at the nuclear bomb test sites. 
In the last three years I have providing evidence in court cases as an expert witness 
for a number of individuals who have suffered cancer as a result of earlier 
exposures. Many of these have been veterans of the nuclear weapons testing carried 



16 



ECRR Proceedings Lesvos 2009 

out by the UK in Australia and Christmas Island. I have to say, that so far, I have 
persuaded the courts in every case that the ECRR model is more accurate than the 
ICRP model, and this despite opposition from expert witnesses from the defence 
side. The cases have thus been won, and in some instances very large settlements 
have resulted. So there is some light at the end of the tunnel. If we can take our 
arguments to the courts, and advance our evidence, it quickly appears that unbiased 
legal minds and juries, presented with this evidence, immediately see that the ICRP 
system of belief is a house of cards, built up in the cold war, and no longer credible 
in the light of modern scientific tests and evidence emerging in the last ten years. 
Much of this evidence has emerged as a result of work by you and our colleagues, 
for which the world should give thanks, and eventually will. 

References 

1. Busby C, (1994) Increase in Cancer in Wales Unexplained, British Medical 

Journal, 308: 268. 

2. Busby C.C. (2009) Very Low Dose Fetal Exposure to Chernobyl Contamination 
Resulted in Increases in Infant Leukemia in Europe and Raises Questions about 
Current Radiation Risk Models. InternationalJournal of Environmental Research 
and Public Health; 6(12):3 105-3 114 

3. Busby, C. C. and Cato, M. S. (2000), 'Increases in leukemia in infants in Wales 
and Scotland following Chernobyl: evidence for errors in risk estimates' Energy and 
Environment 11(2) 127-139 

4. Busby C.C (2003) ed. with Bertell R, Yablokov A, Schmitz Feuerhake I and 
Scott Cato M. ECRR2003: 2003 recommendations of the European Committee on 
Radiation Risk- The health effects of ionizing radiation at low dose— Regulator's 
edition. (Brussels: ECRR-2003); 2004 Translations of the above into French 
Japanese Russian and Spanish (see www.euradcom.org for details) 

5. Yablokov AV, Nesterenko VB and Nesterenko AV (2009) Chernobyl: 
Consequences of the catastrophe for the people and the environment. Edited — 
Janette Sherman-Nevinger. Ann.New.York. Acad. Sciences Vol 1181 

6. Tondel M, Hjalmarsson P, Hardell L, Carisson G, Axelson A, (2004) Increase in 
regional total cancer incidence in Northern Sweden. JEpidem. Community 
Health. 58 1011-1016. 



17 



ECRR Proceedings Lesvos 2009 



7. Loutit JF (1970) Malignancy from Radium. Brit.J.Cancer 24(2) 17-207). 

8. ICRP (2007) ICRP Publication 103: The 2007 recommendations of the 
International Commission on Radiological Protection. Ed J.Valentin. New York: 
Elsevier 

9. Alaani Samira, Tafash Muhammed, Busby Christopher, Hamdan Malak and 
Blaurock-Busch Eleonore (201 1) Uranium and other contaminants in hair from the 
parents of children with congenital anomalies in Fallujah, Iraq Conflict and Health 
2011, 5:15 doi:10.1186/1752-1505-5-15 

10. Busby, Chris; Hamdan, Malak; Ariabi, Entesar. (2010) Cancer, Infant Mortality 
and Birth Sex-Ratio in Fallujah, Iraq 2005-2009. Int. J. Environ. Res. Public Health 

7, no. 7: 2828-2837. 

11. Telegraph 10 th Sept 2009. www.telegraph.co.uk/news/defence/6 1 693 1 8/Ex- 
soildier-died-of-cancer-caused-by-Gulf-War-uranium.html 



18 



ECRR Proceedings Lesvos 2009 



Non cancer illnesses and conditions in areas of Belarus 
contaminated by radioactivity from the Chernobyl 
Accident 

Prof. Yuri Bandashevsky 

Mykolas Romeris University, Vilnius, Lithuania 

The ecological environment influences the health of people and regulates the 
development of human society. Ignoring the considerable overall global progress in 
the business of protection of the environment (and therefore the health of people) 
there are countries in which there are serious environmental problems. First of all 
are the countries of the former Soviet Union. The aspiration to catch up and overtake 
the military and economic development of Western countries forced the former 
Soviet Union administration to introduce new industrial technologies that left a fatal 
impact on the environment and therefore the health of people. First of all, it is 
necessary to consider the Nuclear weapons tests of the USSR. 

Pollution by radioactive elements of huge territories in Belarus, Lithuania, 
Latvia, Estonia, the Ukraine and Russia since the 1960s is the direct consequence. 
The population of these countries had no information on the existing radiation 
factor, and it could therefore not naturally protect itself from its influence in any 
way. 

The Radio-ecological problem in Belarus 

Since the beginning of the 1960s there have been a great number of Cs-137 
radionuclides found in foodstuffs consumed by the inhabitants of these Soviet states 
for many years [1]. Although the contamination of Belarus by the Chernobyl 
catastrophe is well known (Figl) what is less well known is the prior contamination 
by the weapons test fallout. I present a number of pieces of evidence of the 
contamination of areas of the USSR in Figures 2.2-2.4. Fig 2.2 shows how, prior to 
the Chernobyl disaster, Cs-137 levels were high in the 1960s and fell regularly after 
the atmospheric bomb tests were banned in 1963. For example, cow's milk is one of 
the basic products containing high levels of Cs-137 radionuclides for inhabitants of 
Belarus and the Baltic lands. A "Milk-Caesium Map" was created - the largest Cs- 
137 radionuclides contained were observed from 1967 to 1970 in Gomel region of 
the Republic of Belarus. 



19 



ECRR Proceedings Lesvos 2009 




Fig 2.1 Cs-1 37 pollution in territories of Belarus in 1987 



3 

m 

I 

u 



o 
U 




• Russia 

• Belarus 
Ukraine 

• Lithuania 



1964 1965 1966 1967 1968 1969 



Years 



Fig. 2.2 - Cs-1 37 contents in villagers ' daily food allowance in pCi (Marey A.N. and 
co-authors, 1974) 



20 



ECRR Proceedings Lesvos 2009 




Fig. 2.3 Cs-1 37 contents in cow's milk (pCi/l) from different districts of Belarus in 
the 1960s (Marey et al 1974). 

The Chernobyl accident of 1986 intensified a lot the already existing radiation 
effects on the population of many European countries, focusing on the Republic of 
Belarus. The map of Cs-1 37 radionuclides deposition in the territory of Belarus after 
the Chernobyl accident in 1992 (Fig 2.1, Fig 2.4) almost corresponds to the map of 
such radionuclides deposition in the territory of Belarus in the sixties (published in 
1974 (Fig 2.3; Marey A.N. et al. 1974.). It was only due to western public interest 
that after the Chernobyl accident in 1986 it became possible to speak about the 
influence of radiation on the health of people in Belarus and another countries. 
Judged by its scale and consequences, the Chernobyl accident on April 26 1986 is 
considered to be the largest man-caused catastrophe in human history. Its social, 
medical and ecological consequences require detailed study. Above all European 
countries, Belarus was the worst affected. About 70% of the radioactive substances 
released to the atmosphere as a result of the accident at the 4 th block of the 
Chernobyl NPP landed in and contaminated over 23% of the territory of the 
Republic. At present in this zone there live close to 1.4 million inhabitants, including 
260 thousand children. The radiation situation in several affected regions is still 
difficult today. The greatest danger is represented by the consumption of the 
foodstuffs containing radioactive elements Cs-1 37 and Sr-90. The contribution of 
these radionuclides to the internal dose reaches to 70 to 80% (Busby and Yablokov 
2009). The increases in death and reduction in birth rates in Belarus have shown as a 
negative trend in the demography index since 1993: 2002 -5,9%o, 2003 -5,5%o, 2005 
-5,2%o. 



21 



ECRR Proceedings Lesvos 2009 




Fig 2.4 Map ofCs-137 deposition in the territory of Belarus in 1992 




= 



i i i i i i i i i i i i i i i i i i i i i i i i i i i i i i i 

OnOnOnOnOnOnOnOnO^OnOn 



en ^O 

GO GO 
On On 



On <N 
GO On 

On On 



u~, CO 

On On 
On On 



S 3 



O O 



Years 

•Birth rate 



Fig. 2.5 Indices of the death-rate and the birth-rate (per 1000 inhabitants) in the 
Republic of Belarus 



22 



ECRR Proceedings Lesvos 2009 



■c 
= 



25 



20 



15 



X 10 



:- 
SI 

O 

E 

p 



■10 -K 







o en 'O o <n *n oo 

00 00 00 00 G\ 0\ Q\ 
0\ G\ G\ G\ 0\ 0\ 0\ 



s s 



o o 



Years 



Fig 2.6 Demographic index for the Republic of Belarus, 1950-2004 




& .dP S .<# .<# .erf 1 .<*£ .eP) b c^ .«# .«# ^ ^ j& s& j& 



S> V 



S^ \~ 



5T >S 



v 



^ <? 



•Gomel 

■Vetkovski area 
•Narovlianski area 



Years 



V 



^ ^ rfi* 



r^ ^ 



►Grodno 

•Buda-Koshelevski area 
Hoinikski area 



Fig 2. 7 The dynamics of the death-rate of the population in different districts of 
Belarus 



23 



ECRR Proceedings Lesvos 2009 



Diseases of 

organs of 

breath 

3.0% 



Diseases of 

cardiovascular 

system 

52,7% 




Neoplasms 
13.8% 



Diseases of 
digestion 
3,4% Diseases of 
genitourinary 
system 
0.7% 



-External 

reasons 

10.7% 



Other reasons 
14.9% 



Infectious 

diseases 

1,0% 



Fig 2.8 Structure of the causes of death in Belarus, 2008 

Among the causes of death of the inhabitants of Belarus, cardiovascular and 
oncologic diseases take the dominant place. The statistically significant increase in 
the primary incidence of diseases of the cardiovascular system, especially amongst 
those who dealt with the consequences of the Chernobyl nuclear accident is cause 
for anxiety (Fig 2.9). 

Cs-137 radionuclides under conditions of permanent chronic intake in food 
are accumulated in vitally important organs: thyroid gland, heart, kidneys, spleen, 
cerebrum. This affects these organs to different extents. 



24 



ECRR Proceedings Lesvos 2009 



250000 



= 

| 200000 



© 
E 



150000 



100000 



■§ 50000 








n 1 1 r 



n 1 1 1 1 1 1 1 1 



^ j> # j> ^ / / j> ^ # # # # / 

Years 



Fig 2.9 The dynamics of cardiovascular diseases in the Republic of Belarus 



450 



400 



■2 350 



°r 300 



o 250 



-« 200 



150 



"5 100 



50 




*v> *v> S? S? "v* 



-All population 



Years 

-■—City 



cCv J& 



Country 



Fig 2.10 Incidence in the population of the Republic of Belarus of malignant 
neoplasms (per 100,000 inhabitants) 



25 



ECRR Proceedings Lesvos 2009 





o — i (N en 

o o o o 

o o o o 

<N (N (N (N 






Years 



Fig 2.11 The dynamics in the absolute number of cases of thyroid cancer detected 
for the first time in Belarus 




Key: 1 - myocardium, 2 - brain, 3 - liver, 4 - thyroid gland, 5 - kidneys, 6 - spleen, 
7 - skeletal muscles, 8 - small intestine 

Fig 2.12 Cs-137 contents in adults ' and children 's viscera according to the data of 
radiometric measurements of the autopsies of inhabitants of Gomel region in 1997 
and 1998 (Yu. I. Bandazhevsky, 1999, 2003) 



26 



ECRR Proceedings Lesvos 2009 

Cs-137 incorporation leads to metabolism disorders in highly differentiated cells and 
dystrophic and necrobiotic processes in development. The degree of disorder is the 
function of the Cs-137 concentration in the organism and in the organs mentioned 
above. The more intense the process, the higher the degree of disorder. As a rule if 
several organs are subjected to the radiotoxic effects simultaneously, this provokes 
general metabolic dysfunction. It should be noted, the organs and tissues with the 
negligible or absent cell proliferation (e.g myocardium) under physiological 
conditions suffer to the greatest extent. Cs-137, accumulated in the organism, seems 
to block the metabolic processes and affects membrane cell structures. The process 
provokes structure and function disorder in many vital systems but primarily the 
cardiovascular system. Structural, metabolic and functional modifications in the 
myocardium correlate with radiocesium accumulation and demonstrate its toxic 
effects. The energetic system and mitochondrial systems are violated. Deep and 
irreversible changes (due to the increase in Cs-137 concentration) lead to the 
necrobiotic processes in a cell. Suppression of the enzyme creatine phosphokinase 
appears as a consequence of energetic instability (Fig 2.14). 




Fig 2.13 - Accumulation of the rat cardiomiocytes mitochondria with radiocesium 
incorporation 45 Bq/kg Uv. 30 000 



27 



ECRR Proceedings Lesvos 2009 



i control 



i experiment 




Key: 1 - alkaline phosphates, 2 - creatinphosphokinase (p <0,05) 

Figure 2.14 Variations of activities of enzymes in myocardium tissue among 
experimental animals (% versus control) 



The effects of Cs-137 are most extreme in the cardiovascular system of the 
developing organism. Radiocesium concentration over 10 Bq/kg leads to the 
violated electrophysiological processes in the myocardium of children. Those born 
after 1986 and continuously living on the Cs-137 affected territories with 
concentration above 15 Ci/km 2 suffer serious pathological modifications of the 
cardiovascular system, manifesting itself clearly both clinically and electro 
cardiographically. Cs-137 radionuclides incorporation in schoolchildren causes the 
disorder of electrophysiological processes in cardiac muscle shown by the disorder 
of cardiac beat rate. There found to be a clear dependence between the radionuclide 
content in the organism and the cardiac arrhythmia rate (Fig 2.15). 



28 



ECRR Proceedings Lesvos 2009 




0-5 12-26 27-37 38-74 74-100 

137Cs concentration in the organism, Bq/kg 



Fig 2.15 Number of children without ECG modifications as a function of Cs-137 
concentration in the organism (Bandashevsky and Bandashevsky). 



29 



ECRR Proceedings Lesvos 2009 




Fig 2.16 - Histological myocardium composition of a 4 3 -year-old Dobrush resident 
(sudden death case). Radiocesium concentration in heart- 45,4 Bq/kg. Duffisious 
myocytolis. Intermuscular edema. Fragmentation of muscular fibers. Colored by 
hematoxylin and eosin. Uv. X 125 



30 




Figure 2.17 - Histological kidney composition of an albino rat with radiocesium 
concentration 900 Bq/kg. Necrosis and glomerulus fragmentation with cavity 
formation. Necrosis and hyaline-dropping dystrophy of the canaliculus epithelium. 
Colored by hematoxylin and eosin. Uv. X 250 

The situation is quite organ specific. Fig 2.17 shows the effect in the kidney. Due to 
the microscopic architecture of the blood supply the radiation induced pathology of 
the organ has its own specific features. The radiation disease of the kidney is seldom 
accompanied with nephrotic syndromes, but is more severe and quicker in character 
when compared to the ordinary chronic glomerulonephritis. The latter is 
characterized by frequent and early development of the malignant arterial 
hypertension. Already after 2-3 years radiological kidney damage leads to the 
development of chronic renal failure and cerebral and cardiac complications. Kidney 
destruction is one of the main effects of Cs-137 in addition to the products of 
metabolic accumulation in the organism and their toxic effect upon the myocardium 
and other organs and also of the arterial hypertension. If the cases of sudden death in 
Gomel are considered, 89% of these are accompanied by this kind of general organ 
destruction, this state being not registered during their life time. Serious pathological 



31 



ECRR Proceedings Lesvos 2009 

modifications of the liver are also noteworthy. The progress in toxic dystrophy of 
the liver with prevailing destruction of the cellular protein and metabolism 
transformation, results in formation of fat-like substances which contribute to such 
severe pathological processes as fatty hepatosis and cirrhosis (Fig 2.18). 




Fig 2.18 - Histological liver composition of a 40-year-old Gomel resident (sudden 
death rate). Radiocesium concentration in the liver- 142,4 Bq/kg. Fatty and protein 
dystrophy, hepatocytes necrosis. Colored by hematoxylin and eosin. Uv. X 125 



The endocrine system is also exposed to influence of incorporated Cs-137. The 
adrenal gland also appear affected by the incorporated radiocesium, the level of 
Cortisol being a function of the radiocesium concentration in the organism. The 
modifications in Cortisol production are especially noticeable for the neonates, their 
mothers having accumulated considerable Cs-137 concentration in the organisms 
(mainly in the placenta) (Fig 2.19). These children are famous for their ill-adaptation 



32 



ECRR Proceedings Lesvos 2009 

to the intrauterine existence. The effect is seen in rats whose mothers were fed 
Caesium 137 (Figs 2.19, 2.20). 



nmol/l 



3000 
2500 
2000 
1500 
1000 
500 






H mother 



i fetus 



control group 1 group 2 group 3 



Key: Cs- 137 concentration in placenta: Group 1 
Bq/kg; Group 3 - >200 Bq/kg. 



1-99 Bq/kg; Group 2 - 100-199 



Figure 2.19 - Cortisone concentration in mother and foetus blood in control and test 
groups 

Pathology of the female reproductive system is a product of the violation of 
endocrine functions. Radiocesium is also responsible for the imbalance in the 
progesterone-estrogen with women of fertile age in different phases of the oestral 
cycle, and this is a key factor for the infertility. Radiocesium incorporation in 
placenta and other endocrine organs during pregnancy gives rise to hormone 
disorders both in the mother organism and foetus. In particular, the Cs-137 
concentration rising, the testosterone contents increases as well as the thyroid 
hormones and Cortisol in blood. Distortion of hormone statues in the mother- foetus 
system due to radiocesium leads to extended pregnancy time and childbirth and 
postnatal child evolution complications. In case of natural feeding, radiocesium 
penetrates the child's organism. Thus, the mother's organism purifies itself, while 
that of a child's becomes Cs-137 contaminated. Many systems being formed in this 
period, radiocesium has an extremely negative effect upon the child's organism. The 
nervous system is the first to respond to the radioisotopes incorporation. Cs-137 
incorporation within 40-60 Bq/kg, which is due to the 28-days animals feeding with 



33 



ECRR Proceedings Lesvos 2009 

oats, causes distinct imbalance of the biosynthesis of monoamines and neuroactive 
amino-acids in different compartments of the brain, in particular, in the cerebral 
hemispheres, which is characteristic of mean lethal and super lethal radiation doses. 
This is reflected in time of various vegetative disorders. 




Fig 2.0 Rat foetuses from mother fed Cs-137 

The increase of the cases of cataracts in schoolchildren living in the radio 
contaminated areas should also be mentioned - the frequency of detecting this 
pathology is like the other conditions found to be in direct relation to the quantity of 
Cs-137 radionuclides in the organism (Fig 2.21). 



34 



ECRR Proceedings Lesvos 2009 




Fig 2.21- The dynamics of the increase of the cases of cataract in the children of 
Vetka district of Gomel region depending on the level of the average specific activity 
ofCs-137 (Bq/kg) in the organism (Yu.I. Bandazhevsky and co-authors, 1997, 1999) 

To summarise, the long-living radioisotope of Cs-137 affects a number of the vital 
organs and systems. As a result, highly differentiated cells are adversely affected, 
the process being dependent on the radiocesium concentration. The basis of the 
process lies in destruction of the energetic mechanism, leading to protein 
destruction. In this connection, the characteristic feature of the Cs-137 effect upon 
the human organism appears a depressed metabolic processes in the cells of vital 
organs and systems, due to the direct influence and the effects of the toxic tissues 
(nitrogen compounds) and violation of tissue growth due to the vascular system 
disorders. 

The pathological modifications in the human and animals organisms caused 
by Cs-137 may be joined together into a syndrome which may be termed: "long- 
living incorporated radioisotopes". (SLIR). The syndrome appears in the cases of 
radiocesium incorporation in the organism (its degree being the function of the 
incorporation quantity and time) and the syndrome is characterized by the 
metabolism pathology, stipulated for the structural and functional modifications in 
the cardiovascular, nervous, endocrine, immune, reproductive, digestive, urinary 
excretion and hepatic system. The quantity of the radiocesium, inducing SLIR may 
vary, depending on age, sex and the functional condition of the organism. Children 
have been shown to have considerable pathological modifications in the organs and 



35 



ECRR Proceedings Lesvos 2009 

systems with an incorporation level over 50 Bq/kg. Nevertheless, metabolic 
discomfort in the individual systems, primarily in the myocardium, has been 
registered with Cs-137 concentration amounting to 10 Bq/kg. 

Conclusions 

Twenty three years after the accident at the Chernobyl nuclear power plant, the 
inhabitants of the Republic of Belarus, living in the territory contaminated by 
radioactive elements and consuming these radionuclides for a long time, run the risk 
of the incidence by cardiovascular diseases and malignant neoplasms. The steady 
rise of this pathology within 23 years after the accident has led to a situation that is 
close to a demographic catastrophe when a death-rate of the population has begun to 
exceed a birth-rate by a factor of two times. The current situation requires the 
immediate decisions at State and international levels directed at the solution of the 
problem - protecting the state of health of the citizens living in the territories 
affected by the accident at the Chernobyl. 

[1] (Marey A.N. and co-authors, 1974; Rusyayev A.P. and co-authors, 1974; 
Ternov V.I., GurskayaN.V., 1974). 



36 



ECRR Proceedings Lesvos 2009 



Bystander effects and genomic instability Part 1 : From the 
gene to the stream 

Prof. Carmel Mothershill, Prof. Colin Seymour 

McMaster University, Hamilton, Ontario, Canada 

Editors Note: 

Prof Motherhill gave a powerpoint presentation and also later on a paper. Since the 
presentations and remarks at the conference were so interesting we reproduce the 
elements of the presentation as Part I and following this as the paper in Part 2 

I will present our recent research on the phenomena known as genomic instability 
and the bystander effect. Many scientists now refer to these areas as Non Targeted 
Effects NTE. I will consider some aspects and findings relating to Non Targeted 
Effects: 

The fish model 

Case studies 

Serotonin 

DNA repair 

Legacy/ delayed effects 

Multiple stressors 

Implications 

Ecological 

Evolutionary 



The old view of the introduction of genetic damage into somatic cells to cause 
cancer and other effects was that there was a fixed mutation, a hit, and this expanded 
through the normal replication of the cell to increase the number of descendants 
carrying this mutation. This was called the clonal expansion theory. 



37 



ECRR Proceedings Lesvos 2009 

We now believe that this is not an important process and that genomic damage is 
introduced by a different mechanism (Fig 3.1). 

Old view- clonal ^^ — 

0\% «• •: 



Hit 



New view-non-clonal, population-determined outcome 



t 



?Hit 




• <* # 





a% 



Fig 5./ 77ze /m£ between bystander effects and delayed instability 

Genomic instability and bystander effects are linked mechanistically. They occur 
even at very low doses (fully saturated at 5mGy acute dose), and are inducible in 
vivo and in a wide range of species (fish, crustaceans, molluscs as well as 
mammals). The effects are perpetuated in the progeny of those afflicted, and alter 
the chemical uptakes in the bodies. They are detectable by many different endpoint 
measures, including death, survival, proliferation mutation and transformation. 

I will present some examples. 

First, in Fig 3.2 we see that lymphocytes from Chernobyl affected populations 
demonstrate damage 20 years after the exposures. 



38 



ECRR Proceedings Lesvos 2009 



500 



S 300 

g 200 

100 



-f- 



-f- 



Control liquidators PSRER Patients Acute virus 

Lafectlou 
patients 



Fig 3.2 - Damage in lymphocytes from Chernobyl populations 20 years after the 
accident 

Another example comes from experiments with mice. Mitochondrial membrane 
depolarisation effects are shown in Fig 3.6. Below ( Fig 3.3 and 3.4) can be seen 
depolarisation effects in a medium from unirradiated and irradiated tissues from two 
strains of mice. In one (apoptosis prone) damaged cells commit suicide. In the other 
(cancer prone) a signal is initiated which promotes genomic instability. 




Fig 3.3 C57BL/6 apoptosis prone 



39 



ECRR Proceedings Lesvos 2009 











: ? 


, CBA H OGy rTCM 




:.:. 




_ n- CBA H 0.5Gy TCM 




:." 






I.: 






:.: 


m?. m- p i ■ . - 1 ii \i ■ i ■ - v. - : ~t .-.v. v. i r l ■ ■ v ■ V. 1 ■ ■ ■ r v ■ ■ ■ v ■ r - ■ fc ~ 








n ^"""-l- -m wg^B^ggBFP^T 


:.a 






:.: 






Z.2 






:.■ 






: 







a od o ^ w 



1 3 



DO 4~ EM 



CD^CNaooo^HntDo^fN 



time (sec) 



Fig 3. 4 CBA/Ca cancer prone 



-C57BI6 0GylTCM 
-G57BI6 0.5GylTGM 



mTTTTm 




o I 



O ^tf CN 

— cn n 



5 5 



■o m p- id m a> a -- 
time (sec) 



Fig 3.5 C57 Apoptosis prone 



40 



ECRR Proceedings Lesvos 2009 







Fig 3.6 Mitochondrial membrane depolarisation 



140 

120 
C 

1 100 
cd 

* 80 

s 

A 60 
1 40 

20 




i 1 1 


tu 


1 1 






* + * 


T ♦ * 








* **4 


♦-- 






m * T 


♦♦ 


-A- 


A 

1 1 1 1 1 " — i 



0.01 



0.1 



♦ICCM 

Irradiatio 

n 



10 100 

Dose (niGy) 



1000 



10000 



60, 



Fig 3. 7 Bystander and direct dose survival curves over six orders of magnitude Co 
with calcium data 



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ECRR Proceedings Lesvos 2009 



Ionizing radiation 



Ca 2 " 



bystander factor 
molecules 



ROS/Nitric oxide/cytokines 
Biogenic amines 




Fig 3.8 The bystander effect 



It is clear from these findings that a number of questions must be asked. Firstly, can 
we see Non Targeted Effects in other species and can we see them at 
environmentally relevant exposures? Is it possible to see evidence of trans- 
generational effects or mixed exposure effects and finally if so what are the likely 
impacts and how do we deal with them? 



42 



ECRR Proceedings Lesvos 2009 



Purple arrows indicate 
mechanistic break points where 
new, more appropriate, response 
pathways emerge 



Effect 





Zone of "linearity" 



!New "coping" mechanism 



5 aturation 
:ance 



Natural background 



Fig 3.9 Proposed dose response relationship for radiation induced biological effects 



Fundamentally, we must ask if low doses are less or more dangerous than an LNT 
model extrapolation would predict from high doses? 

• Less adaptive response/selection 

• Induced repair/tolerance 

• More 

• GI and bystander effects 

An in-vivo explant model for mechanistic studies can be established. All tissues that 
we have so far tried to date from humans, rodents, fish, frogs, molluscs and prawns 
have yielded viable growing cells capable of producing and responding to bystander 
signals, expressing relevant proteins after irradiation and showing apoptosis and 
necrosis. This differentiation in 2D can also be seen. 



43 



ECRR Proceedings Lesvos 2009 



Measuring bystander response to radiation in vivo 




Irradiate or sham irradiate one fish, 
allow to swim with unexposed 
partner for 2hrs 

Naive fish introduced into 
water from irradiated or sham fish 
After 2hrs 

tissue pieces taken from skin, 

fin, gill, spleen and kidney -do proteomics and tissue 

culture 



Culture of explants for 2 days 



Grow up then examine 
explant outgrowth after 
direct or bystander 
exposure 



Do immunocytochemistry and image 



Harvest culture 
medium 



Add to unirradiated 
clonogenic cell line and 
determine surviving fraction 



reporter assay 



Fig 3.10 Bystander response in vivo 

When these studies were carried out, a number of results pertain. The bystander 
effect was induced in three species of fish exposed to irradiated fish/or their water - 
modeling an evolutionary conserved mechanism. An attenuation of signal was only 
seen after the fish were removed for six hours from the water and live fish continue 
to emit signal for over twelve hours: a stable water soluble signal. The chronically 
exposed Medaka confer an adaptive response on reported cells: The chronic 
radiation effect is different to an acute effect. Multiple stressors appear to have 
sub-additive effects: this suggests a saturable or antagonistic mechanism. 
Bystander proteome and direct irradiation proteome lead to very different results - 
very important for understanding potential risk outcomes. The effect can be 
demonstrated in trout as early as the eyed egg stage and is still there in retested 
adults two years on: it is a persistent effect once induced. Finally, serotonin is 
involved in vivo and in vitro in fish and mammalian cells: a conserved mechanism. 



44 



ECRR Proceedings Lesvos 2009 




BYSTANDER PROTEIN IDENTITIES 



Hemopexin-like protein 



— >0 

My Q < ■ . ■ — — - 

Pyruvate dehydrogenase 

, A Q* 



Unidentified protein 



GDP dissociation inhibitonp 



^ Chromosome 1 SCAF protein 

o« 



i. 




V i 




Fig 3. 11 Bystander protein identities 



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ECRR Proceedings Lesvos 2009 







hhnh I I 



JL 



JlX 



\ \ 



Xr^XXX 



D, Chnomosomel SCAF protein 



ii 



3 

a T a 



\ 



Fig J./2 Proteomic responses to the bystander effect 

Serotonin and DNA repair are critical factors in vivo and in vitro. DNA repairs 
deficient cell lines and transgenic Medaka both produce highly toxic bystander 
signals after low dose irradiation. 



46 



ECRR Proceedings Lesvos 2009 



140 
120 



= 



I 100 

80 1 
_ 60 
# 40 
20 



> 



1 I 



mi i i 

i i i i i i 

i i i i i i i 



*A % 






\ 



& 4l <fc 






*t 



I % control 5HT 
i%bvsta»<ler 



Fig 3.13 Serotonin bound by irradiated cells in vitro, leading to calcium pulse 



47 



ECRR Proceedings Lesvos 2009 




*■ \* & \* %*■ 




IOUeU** 



Fig.3. 14 Reserpine inhibits bystander effect in vitro and in vivo 



48 



ECRR Proceedings Lesvos 2009 




■i.4 i ■; ui 



i 4¥ iiwm-m, i a * 



Fig. 3.15 - Reduced reproductive survival in vitro 



I 



fla ■ 






























m - 












II 


*0 - 












II 


20 - 






1 


d 


ll 


tlJl 




a ■ 


•■ * 


* 

rh 








1 


II 






n _ "> *V ..Or q, 

j-j- 1 A" j&-" fce* .j" 



Fig 3.16 - Increased apoptosis in vivo 



49 



ECRR Proceedings Lesvos 2009 











1. Legacy effect at each subsequent early life stage 
(no additional X-ray dose) 



\ i 



i 




2. Legacy effect after eggs, larvae and first feeders allowed to grow for 1 year 
(with / without an additional 0.5 Gy X-ray dose) 




Fig 3.17 Legacy of early life stage irradiation 

From eyed egg onwards rainbow trout are affected by a 0.5 Gy X-ray dose and an 
X-ray induced bystander effect. Exposure of the egg, larvae and first feeding stages 
results in a legacy of these effects which extends to 1 year old fish. The natures of 
these responses (pro- / anti- apoptotic) are dependent on when the radiation dose 
was administered. We propose these results have implications for the radiological 
protection of the aquatic environment 



50 



ECRR Proceedings Lesvos 2009 



i 













Fig 5./* Legacy effects on copper uptake: Fish exposed to 5mGy acute dose in 
November 2006 as juveniles 



ui 



Ui 



p-un 



Fig 3.19 Legacy effect of 5mGy 2 years ago at egg stage on copper uptake today 



51 



ECRR Proceedings Lesvos 2009 



Irradiate fish 

Metals in water 




o 2 o 



i 



/ \ 



Examine explant 



Dissect fresh tissue from animal 
Do proteomics 

Chop tissue to provide explant pieces 




Culture of explants 



Harvest culture medium containing 

stress signal molecules 



Add to unirradiated 
clonogenic cell line and 
determine survival 
or other stress end points 



Fig 3.20 Measuring radiation induced multiple stressor response in vivo 

A number of multiple stressor fish experiments were carried out (with Norwegian 
collaboration). They offered the conclusion that stress (bystander) signals are 
produced in vivo by salmonids in response to acute or chronic low doses of radiation 
(4-75mGy), and that Al, Cu and Cd all show complex effects when combined with 
low doses of radiation (4-75mGy). Furthermore, tissue specific differences are seen 
with gills being more sensitive than skin. 



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ECRR Proceedings Lesvos 2009 



25 



20 



15 



1 



10 




• Control 
*4mGy alone 

■ low Cu 

■ MedCu 
HighCu 



Skin 



Gill 



Fig 3.21 Effect of4mGy radiation in the presence of copper ions on bystander 
signaling 

But what about some more complex scenarios? Radiation induces a cell to undergo 
apoptosis, removing it from the potentially carcinogenic pool. Substance 2 (eg Cd) 
interferes with the signaling cascade and the cell lives - survival assay suggests that 
there is a protective effect to the interaction. If radiation induces an adaptive 
response in population A, a further stressor has little effect but a pristine population 
B with no adaption is devastated by the same stressor. This effect is clear, but it is 
our response to it that is flawed. Our current approach to risk assessment is dose 
driven, mono-agent and mainly mutation centered, and does not and cannot 
accommodate much of the low dose exposure data available for radiation or 
chemical pollutants. We need an effect (or no effect) driven risk assessment with 
careful regard to predictive value of our chosen reporters. We must learn to 
extrapolate: from effect to harm, harm to risk, individual risk to population risk and 
from population risk to ecosystem risk. We must learn how to regulate with an 
acceptance of uncertainty. However, more than this, there are issues with radiation 
protection studies such as these. Endpoint assays are usually snapshots at best and 
we need lifetime studies and a mechanistic understanding and modeling of factors in 
order to develop a more holistic understanding. This will allow us to validate these 
endpoints across time, and understand the effects of multiple stressors. The new 
non-targeted effects field suggests that low dose effects can fluctuate - so how do 
we live with and regulate in an environment of uncertainty? We must refuse our 
initial desire to cry "no effect", but ask "what effect" and "is it important?". 



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ECRR Proceedings Lesvos 2009 

I finish with a final plea: we must realize that biodiversity (not only of biota) is 
important because we do not fully understand the mechanisms by which stress and 
evolution combine to produce new adaptations. 



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ECRR Proceedings Lesvos 2009 



Part 2: Human and Environmental Health Effects of low 
doses of radiation 

Carmel Motherhill and Colin Seymour 

Department of Medical Physics and Applied Radiation Sciences, McMaster 
University, Hamilton, Ontario, Canada, L8S 4K1 

Abstract 

The last 15 years have seen a major paradigm shift in radiation biology. Several 
discoveries challenge the DNA centric view which holds that DNA damage is the 
critical effect of radiation irrespective of dose. This theory leads to the assumption 
that dose and effect are simply linked - the more energy deposition, the more DNA 
damage and the greater the biological effect. This is embodied in radiation 
protection (RP) regulations as the linear-non-threshold (LNT) model. However the 
science underlying the LNT model is being challenged particularly in relation to the 
environment because it is now clear that at low doses of concern in RP, cells, tissues 
and organisms respond to radiation by inducing responses which are not predictable 
by dose. These include adaptive responses, bystander effects, genomic instability 
and low dose hypersensitivity and are commonly described as stress responses, 
while recognizing that "stress" can be good as well as bad. The phenomena 
contribute to observed radiation responses and appear to be influenced by genetic, 
epigenetic and environmental factors, meaning that dose and response are not simply 
related. The question is whether our discovery of these phenomena means that we 
need to re-evaluate RP approaches. The so called "non-targeted" mechanisms mean 
that low dose radiobiology is very complex and supra linear or hormetic responses 
are equally probable but their occurrence is unpredictable for a given individual. 
Issues which may need consideration are synergistic or antagonistic effects of other 
pollutants because RP at present only looks at radiation dose but the new 
radiobiology means that chemical or physical pollutants which interfere with tissue 
responses to low doses of radiation could critically modulate the predicted risk. 
Similarly, the "health" of the organism could determine the effect of a given low 
dose by enabling or disabling a critical response. These issues will be discussed. 



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ECRR Proceedings Lesvos 2009 



What are "non-targeted" effects 

Within conventional radiobiology as accepted in the 1950's continuing through to 
the 1990's there was little consideration of epigenetic effects, because the traditional 
concept of radiobiology was based on target theory (Timofeeff-Ressovky et al. 
1935, Osborne et al. 2000). For an effect to occur, radiation had to hit a defined 
target within the cell, assumed to be DNA. Assumptions about the number of targets 
hit could then be made from measurements of dose and dose rate (Elkind and 
Whitmore 1967, Alper 1979). The evolution of non-targeted effect (NTE) 
radiobiology meant that at low doses the previous assumptions needed to be 
reconsidered in the light of the existence of non-DNA mechanisms (Morgan and 
Sowa 2006, Mothersill and Seymour 2006, Hei et al. 2008). The mechanisms 
underlying radiation effects are not constant with respect to dose and it would now 
be generally accepted that low dose effects are mechanistically different to high 
doses effects. This is not to say the mechanisms are necessarily mutually exclusive 
but it does mean that NTE's will contribute more to the overall outcome at low 
doses where targeted effects are small. Targeted effects will predominate at high 
doses and in situations where NTE's have been inhibited or otherwise prevented. In 
terms of the progression of radiobiological thinking in this field, disease caused by 
radiation no longer had to be exclusively genetically based, but radiation could 
promote or exacerbate systemic disease. This disease could have been caused for 
example by a chemical mutagen (Preston 2005, Baverstock and Ronkko 2008, 
Gundy 2006). Equally, the radiation could facilitate a non-mutation based 
inflammatory type disease (Kusunoki and Hayashi 2008, Lorimore and Wright 
2003, Manton et al. 2004, Little et al. 2008). These concepts, although largely 
accepted theoretically by the radiobiology community, have been difficult to prove 
epidemiologically because of what are generally called "confounding variables" 
such as smoking, drinking, age, gender, or concurrent past or future exposures to the 
same or a different pollutant (Sigurdson and Ron 2004, Prasad et al. 2004). These 
factors actually reflect the futility of trying to assign causation, as defined in 
epidemiology, to one agent when the doses are low! Others argue that radiation and 
many chemical "pollutants" might actually boost the immune system and be good 
(Calabrese and Baldwin 2000, Sakai 2006, Boonstra et al. 2005). The hormetic 
argument has many interesting applications but is unproven with regard to multiple 
pollutants. This adds to the confusion and controversy surrounding low dose 



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ECRR Proceedings Lesvos 2009 

exposures. The essential point is that there will be huge individual variation due to 
involvement of epigenetic and non-targeted factors in the response (Wright and 
Coates 2006, Pinto and Howell 2007, Fike et al. 2007). At any one time we are as 
unique epigenetically as we are genetically. Epigenetic differences are linked to 
gender and lifestyle. In theory therefore a low dose of radiation could cause any 
number of effects ranging from beneficial to death-inducing disease depending on 
the context of the exposure and the interplay of factors such as cell communication, 
microenvironment, tissue infrastructure and a whole host of systemic variables 
which influence outcome from a cellular track of ionizing radiation (Wright 2007, 
Gault et al. 2007). 

Is radiation unique or is it one of many stressors?? 

Key developments leading to the current widespread acceptance of low doses of 
ionizing radiation as having similar mechanisms to other stressors include 

(1) The development of sensitive techniques such as m-FISH, for detecting 
chromosomal abnormalities. (Pinkel et al. 1988, Speicher et al. 1996, Hande and 
Brenner et al. 2003, Edwards et al. 2005) 

(2) Studies showing that delayed or persistent sub-optimal survival (reproductive 
death) could be seen in surviving progeny of irradiated cells. (Seymour et al, 1986, 
Mothersill and Seymour 1997, Stamato et al. 1987, Coates et al. 2005) 

(3) The emergence of genomic instability as a mechanism by which low doses of 
radiation could cause delayed or persistent damage to chromosomes ( Kadhim et al. 
1992, Little and Nagasawa 1992, Marder and Morgan 1993, Ponniaya et al. 1997, 
Watson etal. 1997). 

(3) The accumulation of knowledge of "bystander effects" whereby chromosome 

damage, death, DNA damage and various other consequences occur in cells 

receiving signals from cells irradiated with low doses of radiation (Hei 2004, 

Lorimore et al. 1998, Brenner et al. 2001, Schettino et al. 2005, Weber et al. 2005, 

Lui et al. 2006). 

(4). Criticism of the epidemiological research undertaken after the Hiroshima and 

Nagasaki bombs as ignoring the damage from residual radiation and fall out 

(Sawada 2007, Mossman 2001). 

The NTE paradigm emerged initially as a result of re examination of firmly held 

beliefs and some odd results in the laboratory which did not fit the DNA paradigm. 

Proof of the new hypotheses required the techniques such as molecular imaging, M- 



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ECRR Proceedings Lesvos 2009 

FISH, and SKY as well as the development of tissue culture techniques for human 
normal tissues which permitted functional studies to be performed (Freshney 2005). 
Older studies tended to use high doses on a limited number of cell lines or highly 
inbred animal strains. These tended to thrive in the laboratory but were often 
unrepresentative of tissues in the outbred human or non-human (Elkind 1988, 
Hornsey et al. 1975, Alper 1973). 

Important consequences for radiation protection and risk assessment: of newly 
discovered low dose effects 

1. Life is organized in hierarchies of organisation 

Hierarchical levels stretch from the individual "down" (organs - tissues - cells - 
organelles -genes ) and "up" to populations (multiples individuals/ single species 
(multiples species - ecosystems). Confusion in the low dose exposure field (both 
radiation and chemical) arise from lack of consideration of this concept. Most of the 
arguments about whether radiation is "good" or "bad" fail due to lack of 
consideration of the level at which the effects occur and because most of the 
arguments are really only able to rely on human cancer incidence or deaths for data. 
For example cell death is seen as a "bad" effect but if it removes a potentially 
carcinogenic cell from the population of cells in a tissue it could prevent cancer 
starting and could be seen as "good". Survival of cells is seen sometimes as "good" 
but if they survive with unrepaired or wrongly repaired damage, they could start or 
facilitate development of a cancer. Similarly in the non-human populations - death 
of radiosensitive individuals which cannot adapt to the changed (now 
radioactive/chemically polluted) environment, could be "good" for the population in 
evolutionary terms depending on the life stage and reproductive status when the 
effects manifest, although death will always be "bad" for the individual. It is only 
by considering responses in context, that any conclusions can be drawn about risk or 
harm. 

2. Concepts related to time and space 

There are two aspects to this - one is simply, the age of the organism at the time of 
irradiation and the deposition pattern of the ionizing energy (its linear energy 
transfer or LET). This concept is relevant across all hierarchical levels. Obvious 
considerations are the age or maturity of the individual entity which gets irradiated, 



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ECRR Proceedings Lesvos 2009 

the density of the energy deposition, the lifetime of the entity and its importance in 
the context of functionality of the higher hierarchical levels. Young entities are 
usually less stable and more vulnerable (or more adaptive?) than old entities because 
of their faster metabolic rate, higher rate of growth/cell division and at the 
ecosystem level, because of their less strongly developed interdependencies. There 
is also more capacity to absorb change in young entities, for example there are more 
available individuals, better reproductive rates and better viability from young 
parents , whether cells or organisms. The other aspect is that the delayed effects of 
radiation and bystander effects mean that radiation effects are not fixed in time or 
space to the energy deposition along ionizing track. The effects can persist and 
manifest at distant points in time and space. These concepts are also discussed 
elsewhere (Preston 2005, Baverstock and Ronkko 2008). 

3. The importance of mixed exposure analysis 

Pollutants including radiation seldom occur in isolation. In fact most environmental 
radioactivity comes from radioisotopes which are chemical entities. This means that 
there is always a mixed exposure and that both the chemical and radioactive aspects 
need to be considered. Additive damage used to be an acceptable way to deal with 
mixed exposures (if any were used!). The new field of non-targeted effects with the 
consequent realization that emergent properties can exist, which were not 
predictable from the individual agent dose response data, makes this no longer 
acceptable. The complexities of mixed pollutant scenarios call for a re-think of 
fundamental approaches to both epidemiological causation after low dose exposures 
to anything. They also question the need regulators have to regulate to a number 
(dose unit/exposure unit). Some of the issues concerning the latter position include 
the following: 

• How to ensure compliance if there is no "safe" or legal limit? 

• How to deal with multiple stressors especially if the interactions are not 
known? 

• How to correct for dose rate/ time of exposure? - DDREF values are clearly 
not effective. 

• How to deal with mixed chronic and acute exposures? 

• How to factor in possible hormetic, adaptive, or antagonistic effects? 

• How to regulate in pristine versus dirty environments? 



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ECRR Proceedings Lesvos 2009 

The issues of legal causation are highly relevant to the former point but outside the 
scope of this review. Discussion of these issues can be found elsewhere (Masse 
2000, Gonzalez 2005, Miller 2006). Ultimately, in order to resolve these issues, 
more data are needed for mixed exposure senarios using relevant species. Systems 
biology approaches involving close interaction between experimental biologists and 
modellers are also required. 

Data concerning low dose effects of multiple stressors 

There are very little data where low dose exposures to multiple stressors/mixed 
contaminants involving radiation and a chemical are investigated. The field was 
reviewed by Mothersill et al. (Mothersill et al. 2006). Recent interest in non- 
targeted effects probably means more attention will be paid to this area in future. 
Gowans et al. (Gowans et al. 2005) have data showing chemical induction of 
genomic instability. Data from the authors' own and other laboratories shows that 
heavy metals singly or in combination can cause genomic instability (Grygoryev et 
al. 2008, Bagwell et al. 2008, Mothersill et al. 1998, Dowling et al. 2005, Dowling 
and Mothersill 2001, Ni Shuilleabhain et al. 2006, Dowling and Mothersill 1999, 
Mothersill et al. 2001, Lyng et al. 2004, Glaviano et al. 2006, Glaviano et al. 2009, 
Coen et al. 2003, Coen et al. 2001). Delayed death and chromosome aberrations in 
human cells following nickel, titanium or cadmium exposure have been reported 
(Glaviano et al. 2006, Glaviano et al. 2009, Coen et al. 2003, Coen et al. 2001). 
Similar effects have been reported in fish cell lines [Dowling et al. 2005, Dowling 
and Mothersill 2001, Ni Shuilleabhain et al. 2006, Dowling and Mothersill 1999, 
Mothersill et al. 2001, Lyng et al. 2004], and more recently in live fish exposed to 
very low doses of gamma radiation 4-75mGy over 48hrs in the presence of heavy 
metals at levels just above background (Salbu et al. 2008, Mothersill et al. 2007). 
Organic pesticides and detergents such as prochloras, nonoylphenol, nonoxynol and 
dichloroaniline have also been found to cause delayed lethal mutations in fish cells 
(Mothersill et al. 1998, Dowling et al. 2005, Dowling and Mothersill 1999). 
Chromium and vanadium used in implants and dentures lead to a variety of genetic 
and reproductive delayed effects in vivo and to multiple endpoints associated with 
non-targeted effects in vitro (Glaviano et al. 2006, Glaviano et al. 2009, Coen et al. 
2003, Coen etal. 2001). 



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ECRR Proceedings Lesvos 2009 

What does this mean for environmental protection and human health? 

While many of the studies cited above are concerned with fish rather than humans, 
the data show that non-targeted effects can be induced by low dose exposures to a 
number of environmental chemicals as well as ionizing radiation. This means that 
combined exposures to low doses of these agents cannot be regulated in isolation 
and that studies of potential mechanistic interactions are important. Radiation 
protection of humans could find use from the approaches which are being taken by 
the task groups within ICRP, IAEA and the US-DoE (see for example ICRP 
Publication 91, ICRP Publication 103 2009) who have to formulate policy to 
regulate exposure of non-human biota. Many of the issues involved such as dealing 
with non-cancer endpoints, mixed contaminants or chronic low dose exposure are 
real issues in human radiation protection. 

Conclusions and summary 

The challenge in the low dose exposure field is to tease out the "noise". Noise is the 
euphemistic term we use when the level of the disease which is un-attributable to 
our favoured causative agent, is too high to prove causation formally in any strict 
scientific or legal sense. Perhaps we should accept that we cannot assign causation 
and instead view ionizing radiation as one among many agents which together 
contribute to cause disease. Before we can do this it is vital to understand the key 
mechanisms and in particular to find areas of mechanistic commonality suggesting 
common causation. Biomarkers may be useful to identify possible common 
mechanisms and to validate their relevance across different hierarchical levels. If 
this is achieved it should be possible to model links between effects at one level e.g. 
cellular or individual leading to harm and risk at higher levels - in this example the 
individual or the population. Biomarker studies do need to be interpreted cautiously 
however because they are often used as surrogates for risk when in fact they may 
merely be pointing to change in the system. Without the back-up modeling and 
multi-level analysis of their relevance they may lead to false conclusions and 
confusion about the true risk of an inducing agent. 

The problem of establishing causation following mixed exposures remains 
along with the issue of what constitutes "harm". In the non-human biota field, there 
is great concern about doing more harm than good, if action levels are enforced 
which might require "remediation" of a habitat - i.e. removal of contaminated 



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ECRR Proceedings Lesvos 2009 

vegetation and soil. This could cause much more harm to the ecosystem than the 
original stressor. In the realm of human protection against low dose stressors, issues 
might include the ethics of genetic screening to identify sensitive sub-populations. If 
a sensitivity marker were available, who should be tested and when? Should 
diagnostic screening be forbidden to these individuals because of their possible 
sensitivity to low doses of radiation? There are also issues regarding lifestyle 
choices and risk benefit analysis at the biological level. Evolutionary adaptation 
leads to a fitter population (of cells, individuals) by eliminating the weak units but 
how is that population changed? 

It would be nice to conclude this paper with a "way forward" but as we are 
still in the very early stages of accepting that radiation doses effects at low doses are 
non-linear, that multiple stressors impact the final outcome, and that what appears to 
be bad (or good) may be good (or bad)- it is perhaps best to recommend caution and 
consideration of these points rather than changing the regulatory framework! 

References 

Alper T. 1973. The relevance of experimental radiobiology to radiotherapy. 
Present limitations and future possibilities British Medical Buletin. 29:3-6 

Alper, T. 1979. Cellular Radiobiology Cambridge University Press 
(Cambridge:UK) 

Bagwell CE, Milliken CE, Ghoshroy S, Blom DA. 2008. Intracellular copper 
accumulation enhances the growth of Kineococcus radiotolerans during chronic 
irradiation Applied and Environmental Microbiology. 74:1376-1384 

Baverstock K, Ronkko M. 2008. Epigenetic regulation of the mammalian cell 
PLoS ONE 4;3 e2290 

Boonstra R, Manzon RG, Mihok S, Helson JE. 2005. Hormetic effects of 
gamma radiation on the stress axis of natural populations of meadow voles 
(Microtuspennsylvanicus) Environmental Toxicology & Chemistry 24:334-343 

Brenner D.J. et al. 2001. The bystander effect in radiation oncogenesis 
Radiation Research 155:402-8:13 



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Calabrese EJ, Baldwin LA. 2000. The effects of gamma rays on longevity 
Biogerontology 1:309-319 

Coates PJ, Lorimore SA, Wright EG. 2005. Cell and tissue responses to 
genotoxic stress Journal of Plant Pathology 205:221-235 

Coen N, Kadhim MA, Wright EG, Case CP, Mothersill CE. 2003. Particulate 
debris from a titanium metal prosthesis induces genomic instability in primary 
human fibroblast cells. British Journal of Cancer 88:548-552 

Coen N, Mothersill C, Kadhim M, Wright EG. 2001. Heavy metals of relevance 
to human health induce genomic instability Journal of Plant Pathology 195:293- 
299 

Dowling K and Mothersill C. 1999. Use of rainbow trout primary epidermal cell 
cultures as an alternative to immortalized cell lines in toxicity assessment: a 
study with nonoxynol Environmental Toxicology and Chemistry 18:2846-2850 

Dowling K and Mothersill C. 2001. The further development of rainbow trout 
primary epithelial cell cultures as a diagnostic tool in ecotoxicology risk 
assessment Aquatic Toxicology 53:279-289 

Dowling K, Seymour C, Mothersill C. 2005. Delayed cell death and bystander 
effects in the progeny of Chinook salmon embryo cells exposed to radiation and 
a range of aquatic pollutants International Journal of Radiation Oncology 
Biology Physics. 81:89-96 

Edwards AA.et al. 2005. Review of translocations detected by FISH for 
retrospective biological dosimetry applications Radiation Protection Dosimetry 
113:396-402 

Elkind MM. 1967. Radiobiology of Cultured Mammalian Cells Gordon and 
Breach Science Publishers 



63 



ECRR Proceedings Lesvos 2009 

Elkind MM. 1988. The initial part of the survival curve: does it predict the 
outcome of fractionated radiotherapy? Radiation Research 1 14:425-436 

Fike JR, Rola R, Limoli CL. 2007. Radiation response of neural precursor cells 
Neurosurgery Clinics of North America 18:115-127 

Freshney RI. 2005. Culture of Animal Cells a manual of basic technique Wiley 
(Liss, USA) 

Gault N, Rigaud O, Poncy JL, Lefaix JL. 2007. Biochemical alterations in 
human cells irradiated with alpha particles delivered by macro- or microbeams 
Radiation Research 167:551-562 

Glaviano A, Mothersill C, Case CP, Rubio MA, Newson R, Lyng F. 2009. 
Effects of hTERT on genomic instability caused by either metal or radiation or 
combined exposure. Mutagenesis 24:25-33 

Glaviano A, Nayak V, Cabuy E, Baird DM, Yin Z, Newson R, Ladon D, Rubio 
MA, Slijepcevic P, Lyng F, Mothersill C, Case CP. 2006. Effects of hTERT on 
metal ion-induced genomic instability Oncogene 25:3424-3435 

Gonzalez A J. 2005. Lauriston S. Taylor Lecture: Radiation protection in the 
aftermath of a terrorist attack involving exposure to ionizing radiation Health 
Physics 89:418-446 

Gowans ID, Lorimore SA, Mcllrath JM, Wright EG. 2005. Genotype-dependent 
induction of transmissible chromosomal instability by gamma-radiation and the 
benzene metabolite hydroquinone Cancer Research. 65:3527-3530 

Grygoryev D, Moskalenko O, Zimbrick JD. 2008. Non-linear effects in the 
formation of DNA damage in medaka fish fibroblast cells caused by combined 
action of cadmium and ionizing radiation Dose Response 6:283-298 

Gundy S. 2006. The role of chemical and physical factors in cancer 
development Magyar Onkologia 50:5-18 



64 



ECRR Proceedings Lesvos 2009 

Hande M.P, Brenner D.J.et al. 2003. Past Exposure to densely ionising radiation 
leaves a unique permanent signature in the genome The American Journal of 
Human Genetics 72:1162-1170 

Hei TK, Persaud R, Zhou H, Suzuki M. 2004. Genotoxicity in the eyes of 
bystander cells Mutation Research. 568:1 1 1-120 

Hei TK, Zhou H, Ivanov VN, Hong M, Lieberman HB, Brenner DJ, Amundson 
SA, Geard CR. 2008. Mechanism of radiation-induced bystander effects: a 
unifying model Journal of Pharmacy and Pharmacology 60:943-950 

Hornsey S, Kutsutani Y, Field SB. 1975. Damage to mouse lung with 
fractionated neutrons and x rays Radiology 1 16:171-174 

ICRP Publication 103. 2009. New Recommendations of the ICRP. Annals of the 
ICRP 

ICRP Publication 91. A framework for assessing the impact of ionising radiation 
on non-human species. Annals of the ICRP 33(3):20 1-270 
ICRP. 37(2-4) Elsevier BV. 

Kadhim MA , Macdonald DA, Goodhead DT, Lorimore SA, Marsden SJ, Wright 
EG . 1992. Transmission of chromosomal instability after plutonium alpha- 
particle irradiation Nature 355:738-740 

Kusunoki Y, Hayashi T. 2008. Long-lasting alterations of the immune system 
by ionizing radiation exposure: implications for disease development among 
atomic bomb survivors International Journal of Radiation Oncology Biology 
Physics 84:1-14 

Little JB, Nagasawa H. 1992. Induction of sister chromatid exchanges by 
extremely low doses alpha-particles Cancer Research 52:6394-6396 

Little MP, Tawn EJ, Tzoulaki I, Wakeford R, Hildebrandt G, Paris F, Tapio S, 
Elliott P. 2008. A systematic review of epidemiological associations between 
low and moderate doses of ionizing radiation and late cardiovascular effects, and 



65 



ECRR Proceedings Lesvos 2009 

their possible mechanisms Radiation Research 169:99-109 

Lorimore SA, Kadhim MA, Pocock DA, Papworth D, Stevens DL, Goodhead 
DT, Wright EG. 1998. Chromosomal instability in the descendents of 
unirradiated surviving cells after alpha-particle irradiation Proceedings of the 
National Academy of Sciences 95:5730-5733 

Lorimore SA, Wright EG. 2003. Radiation-induced genomic instability and 
bystander effects: related inflammatory-type responses to radiation-induced 
stress and injury? Int J Radiat Biol. 79:15-25 

Lui Z, Mothersill CE, McNeill FE, Lyng FM, Byun SH, Seymour CB, Prestwich 
WV .2006. A dose threshold for a medium transfer bystander effect for a human 
skin cell line Radiation Research 166:19-23 

Lyng FM, Lyons-Alcantara M, Olwell P, Ni Shuilleabhain S, Seymour C, 
Cottell DC, Mothersill C. 2004. Ionizing Radiation Induces a Stress Response in 
Primary Cultures of Rainbow Trout Skin Radiation Research 162:226-232 

Manton KG, Volovik S, Kulminski A. 2004. ROS effects on neurodegeneration 
in Alzheimer's disease and related disorders: on environmental stresses of 
ionizing radiation Current Alzheimer Research 1 :277-293 

Marder BA, Morgan WF. 1993. Delayed chromosomal instability induced by 
DNA damage Molecular and Cellular Biology 13:6667-6677 

Masse R. 2000. Ionizing radiation C R Acad Sci III 323(7) 633-40 

Miller C. 2006. Causation in personal injury: legal or epidemiological common 
sense? Legal Studies 26:544-569 

Morgan WF, Sowa MB. 2006. Non-targeted bystander effects induced by 
ionizing radiation Mutation Research 616:159-164 Epub 

Mossman KL. 2001. Deconstructing radiation hormesis Health Physics 80:263-9 



66 



ECRR Proceedings Lesvos 2009 



Mothersill C, Crean M, Lyons M, McSweeney J, Mooney R, O'Reilly J, 
Seymour CB. 1998. Expression of delayed toxicity and lethal mutations in the 
progeny of human cells surviving exposure to radiation and other environmental 
mutagens International Journal of Radiation Oncology Biology Physics 74:673- 
680 

Mothersill C, Lyng F, Mulford A, Seymour C, Cottell D, Lyons M , Austin B. 
2001. Effect of Low Doses of Ionizing Radiation on Cells Cultured from the 
Hematopoietic Tissue of the Dublin Bay Prawn, Nephrops norvegicus Radiation 
Research 156:241-250 

Mothersill C, Salbu B, Heier LS, Teien HC, Denbeigh J, Oughton D, Rosseland 
BO, Seymour CB. 2007. Multiple stressor effects of radiation and metals in 
salmon (Salmo salar) Journal of Environmental Radioactivity 96:20-31 

Mothersill C, Seymour C. 1997. Lethal mutations and genomic instability 
International Journal of Radiation Oncology Biology. 71:751-758 

Mothersill C, Seymour C. 2006. Radiation-induced bystander and other non- 
targeted effects: novel intervention points in cancer therapy? Current Cancer 
Drug Targets 6:447-454 

Mothersill, C Mosse, I Seymour, CB. 2006. Proceedings of the NATO 
Advanced Research Workshop on Multipollution Exposure and Risk 
Assessment - A Challenge for the Future, Minsk, Belarus, 1-5 Multiple 
Stressors: A Challenge for the Future 6:283-298 Epub 2007 ISBN: 978-1-4020- 
6334-3 

Ni Shuilleabhain S, Mothersill C, Sheehan D, O'Brien NM,0' Halloran J, van 
Pelt FN, Kilemade M, Davoren M. 2006. Cellular responses in primary 
epidermal cultures from rainbow trout exposed to zinc chloride Ecotoxicology 
and Environmental Safety 65:332-341 

Osborne James C, Miller Jr, Jay H., and Kempner ES. 2000. Molecular Mass 
and Volume in Radiation Target Theory Biophysical Journal 78: 1698 -1702 



67 



ECRR Proceedings Lesvos 2009 



Pinkel et al. 1988. Fluorescence in situ hybridization with human chromosome- 
specific libraries: Detection of trisomy 21 and translocations of chromosome 4 
Proceedings of the National Academy of Sciences 85:9138-9142 (USA) 

Pinto M, Howell RW. 2007. Concomitant quantification of targeted drug 
delivery and biological response in individual cells Biotechniques 43:64, 66-71 
PMID: 17695254 

Ponniaya B et al. 1997. Radiation-induced chromosomal instability in BALB/c 
and C57BL/6 mice: the difference is as clear as black and white Radiation 
Research 147:121-125 

Prasad KN, Cole WC, Hasse GM. 2004. Health risks of low dose ionizing 
radiation in humans: a review Experimental Biology and Medicine 229:78-82 

Preston RJ. 2005. Bystander effects, genomic instability, adaptive response, and 
cancer risk assessment for radiation and chemical exposures Toxicology and 
Applied Pharmacology 1:550-556 

Sakai K. 2006. Biological responses to low dose radiation—hormesis and 
adaptive responses Yakugaku Zasshi 126:827-831 

Salbu B, Denbeigh J, Smith RW, Heier LS, Teien HC, Rosseland BO, Oughton 
D, Seymour CB, Mothersill C. 2008. Environmentally relevant mixed exposures 
to radiation and heavy metals induce measurable stress responses in Atlantic 
salmon Environmental Science & Technology 42:3441-3446 

Sawada S. 2007. Cover-up of the effects of internal exposure by residual 
radiation from the atomic bombing of Hiroshima and Nagasaki Medicine, 
Conflict and Survival 23:58-74 

Schettino G, Folkard M, Michael BD, Prise KM. 2005. Low-dose binary 
behaviour of bystander cell killing after microbeam irradiation of a single cell 
with focused c(k) x-rays Radiation Research 163:332-336 



68 



ECRR Proceedings Lesvos 2009 

Seymour CB, Mothersill C, Alper T. 1986. High yields of lethal mutations in 
somatic mammalian cells that survive ionizing radiation International Journal of 
Radiation Biology & Related Studies in Physics, Chemistry & Medicine 50:167- 

79 

Sigurdson AJ, Ron E. 2004. Cosmic radiation exposure and cancer risk among 
flight crew Cancer Invest 22:743-761 PMID: 15581056 

Speicher et al. 1996. Multiple-fluorescence in situ hydridisation for chromosome 
karyotyping Nature Protocols 1 : 1 172-1 1 

Stamato T, Weinstein R, Peters B, Hu J, Doherty B, Giaccia A. 1987. Delayed 
mutation in Chinese hamster cells Somatic Cell and Molecular Genetics 13:57- 
65 

Timofeeff-Ressovky, N. W., Zimmer K. G., and Delbriick M. 1935. Uber die 
Natur der Genmutation und der Genstruktur, Nachrichten von der Gesellschaft 
der Wissenschaften zu Gottingen Mathematische-Physikalische Klasse, 
Fachgruppe VI, Biologie 1:189-245 

Watson GE, Lorimore SA, Clutton SM, Kadhim MA, Wright EG. 1997. Genetic 
factors influencing alpha-particle-induced chromosomal instability International 
Journal of Radiation Oncology Biology Physics 71:497-503 

Weber TJ, Siegel RW, Markillie LM, Chrisler WB, Lei XC, Colburn NH. 2005. 
A paracrine signal mediates the cell transformation response to low dose gamma 
radiation in JB6 cells Molecular Carcinogenesis 43:31-37 

Wright EG. 2007. Microenvironmental and genetic factors in haemopoietic 
radiation responses Journal of Radiation Oncology Biology Physics 83:813-818 

Wright EG, Coates PJ. 2006. Untargeted effects of ionizing radiation: 
implications for radiation pathology Mutation Research 11:119-132 



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5 

How reliable are the dose estimates of UNSCEAR for 

populations contaminated by Chernobyl fallout? A 

comparison of results by physical reconstruction and 

biological dosimetry. 

Inge Schmitz-Feuerhake 

University of Bremen, Germany 

According to the United Nations Committee on the Scientific Effects of Atomic 
Radiation UNSCEAR which is adopted by the World Health Organisation WHO in 
evaluating the sequels of the Chernobyl accident the average dose of the population 
in the contaminated regions was very low - except for the thyroid in the nearby 
countries. The main contributions for the other tissues are thought to be generated - 
externally and internally - by the cesium isotopes 137 and 134. Relevant nuclides 
for the exposure as Sr-90 and Pu-239 are assumed to be negligible in distances 
greater than 100 km from the plant. Even for highly contaminated regions outside 
the evacuation zone where more than 37 kBq/m 2 of Cs-237 surface activity were 
measured the mean effective dose was estimated to only about 10 mSv. For the 
neigbouring country of Turkey und the Central European countries in greater 
distances the estimated exposures remain below 1.2 mSv (effective dose). 

These results are in contradiction to findings by biological dosimetry. 
Several research groups investigated radiation-specific cytogenetic alterations in the 
lymphocytes of persons in the contaminated regions directly after the accident or 
some years later. The majority of studies revealed that the rate of unstable and stable 
chromosome aberrations is much higher - by up to about 1 to 2 orders of magnitude 
- as would be expected if the physically derived exposures were correct. A further 
finding was the occurrence of multiaberrant cells which indicate a relevant 
contribution of incorporated alpha activity. Emitted nuclear fuel and breeding 
products should therefore be considered in the physical dose calculations. 



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ECRR Proceedings Lesvos 2009 



Introduction 



Many observations about cancer and other radiation effects in the populations 
affected by Chernobyl fallout are denied by UNSCEAR and other international 
committees refering to the very low exposures which were derived by physical 
considerations. It is therefore important to realize that numerous reports in the 
literature show different results. The authors base their estimates either on own 
calculations or on EPR measurements in teeth or on cytogenetic studies which have 
been applied for the purpose of biological dosimetry. 

We have compiled data about radiation-induced chromosome aberrations because 
they allow an assessment whether the physically derived value will grossly 
underestimate the true exposure. Some thousand persons have been investigated in 
the contaminated regions by cytogenetic methods who can be considered as random 
sample of the population living there. For such comparison, we prefer the results 
about dicentric chromosomes in the lymphocytes together with centric rings. These 
aberrations can be regarded as radiation-specific (Hoffmann and Schmitz-Feuerhake 
1999). 

Dicentric chromosomes are used as biological dosimeter since decades (Fig.l). 
They are instable, i.e., they leave the system with half-lives of about 1.5 years. The 
reason is that they fail to undergo a division in about 50 % of cases because of the 
two centromers. The advantage is, however, that the background rate remains low. 
Further, the background rate is almost constant over the world (only about 4 
dicentric chromosomes in 10.000 metaphases of adults, 1 in 100.000 of children). 
Therefore, the method is very sensitive. The doubling dose is about 10 mSv for an 
acute and homogeneous whole body exposure. But even this method would show no 
significant elevation in a population if the average additional dose does not exceed a 
few mSv. 

Centric rings (cr) are usually counted together with the dicentric chromosomes 
(die). They are originated by the same primary mechanism. They undergo division 
without loss and thus they are stable, but they are generated less frequently (only 
10% in comparison to die). Sometimes, it is therefore possible to derive from the 
relation between cr and die that the exposure occurred far back in the past. 

The application of dose-effect relationships for chromosome aberrations demands 
an homogeneous whole body exposure which is usually not fulfilled in the case of 
incorporated radioactivity. The element cesium is, however, considered to distribute 
homogeneously in the body. Therefore, if the exposure is mainly generated by Cs 



71 



ECRR Proceedings Lesvos 2009 

134 and Cs 137 - externally and internally - as claimed by UNSCEAR, the method 
can be used to decide whether the calculated dose values are realistic. 

Another important information is given by the distribution of the aberrations 
among the cells. For low doses, a low LET radiation (gamma, x-rays) leads to a 
Poissonian distribution of the die, i.e., there is usually only one die per cell. If an 
overdispersion appears, i.e., a clustering of die and/or multiple aberrations in a cell, 
it is an indication for densely ionizing radiation. 



*7 / 


to W ^ m m/L 


* n » *s * 




* 4/ .-* 



Fig. 5.1 Dicentric chromosomes (black arrows) in a human metaphase and 
associated acentric fragments after high dose exposure (from Fritz-Niggli 1997) 

We refer also to results of the studies about reciprocal translocations in lymphocytes 
(visualized by FISH) which are used to estimate the accumulated dose because these 
aberrations are also stable. The background rate is, however, highly variable and 
accumulating with age, therefore the sensitivity is not always sufficient to evaluate 
exposures by environmental radioactivity. 



72 



ECRR Proceedings Lesvos 2009 

Chromosome aberration studies in evacuees 

One day after the accident 45.000 inhabitants were evacuated from Prypiat, further 
90.000 persons from the 30 km zone 7-9 days later (Imanaka and Koide 2000). The 
evacuation was finished 18 days after the accident. The evacuees were therefore 
exposed to very different degree. Among them acute radiation effects were 
registered by official report which means that whole body doses above 1 Sv have 
been reached. 

A mean effective dose estimate for this population of 14 mSv is reported by 
UNSCEAR and WHO (UN 2005). The external dose alone was derived by Imanaka 
and Koide (2000) to 20-320 mSv. An estimate of Prohl et al. (HP 2002) including 
the internal exposure lead to values for adults between 6 and 330 mSv and for the 1 
year old child between 13 and 880 mSv. 

Results of chromosome aberration studies in random samples of the evacuees are 
shown in table 5. 1. All investigations show significant elevations of the mean rate 
of dic+cr even when they were carried out several years after the main exposure. 
Elevation factors of 3 to 100 correspond to at least mean doses of 20 mSv to 1 Sv 
assuming homogeneous whole body exposure. Maznik and coworkers derive a mean 
dose of about 400 mSv for the evacuees from their chromosome studies which is 
higher by a factor 30 than the value given by UNSCEAR. 

Chromosome studies in highly contaminated regions 

Tables 5.2 and 5.3 show the results of chromosome studies in highly contaminated 
regions. They also exceed by far the physical dose estimates assumed by 
UNSCEAR. Remarkable is the appearance of overdispersion and multiaberrant cells 
which proves a significant contribution of incorporated alpha activity 



73 



ECRR Proceedings Lesvos 2009 

Table 5.1 Biological dosimetry in evacuees from the 30 km zone 
Die dicentric chromosomes, cr centric rings 



Region 


Sample 


Date of 

investiga- 
tion 


Method 


Results 
Mean 
elevation& 
specialities 


Authors 


Remarks 


Evacuees 
from 
Prypiat 
and nearby 


43 adults 


1986 


Die 


18-fold 

No 
overdispersion 


Maznik et 
al. 1997 


Result of 
the cited 
authors 
430 mSv 


Evacuated 
zone 


60 
children 


1986 


Dic+cr 


15-fold 

No 
overdispersion 


Mikhalevich 
et al. 2000 


Result of 
the cited 
authors 
400 mSv 


Evacuees 
from 
Prypiat 
and nearby 


102 
adults 

10 
children 


1987- 
2001 


Dic+cr 


Maximum 18- 
fold in 
1987,then 
decline but 
staying sign, 
elevated 


Maznik 
2004 


Result of 
the cited 
author 
360 mSv 


Evacuated 
zone 


244 
children 


1991 


Dic+cr 


circ 100- 
fold*) 


Sevan 'kaev 
etal. 1993 


Dose 

calculation 

IAEA 

(1991) 1-8 
mSv 


Evacuated 

from 

Pripyat 


24 
children 


1991- 
1992 


Die 


circ 3-fold*) 


DeVita et 
al. 2000 




Evacuated 
zone 


12 adults 


1995 


Dic+cr 


7-10 fold*) 


Pilinskaya 
etal. 1999 




Evacuation 
zone, 

residents 


33 adults, 

not 

evacuated 


1998- 
1999 


Dic+cr 


5.5-fold 


Bezdrobnaia 
et al. 2002 





*) estimation by the writers 



74 



ECRR Proceedings Lesvos 2009 



Table 5.2 Biological dosimetry in inhabitants of Gomel and Gomel region 



Die dicentric chromosomes, cr centric rings 



Tralo translocations 



Sample 


Date of 

investiga- 
tion 


Method 


Results 

Mean elevation 

& specialities 


Authors 


Remarks 


43 pregnant 


1986- 


Dic+cr 


5-fold 


Feshenko et 




women 


1987 




40-fold 


al. 2002 




18 infants 












8 persons 


1988- 


Dic+cr 


circ 40-fold*) 


Serezhenkov 


Comparison 




1990 






etal. 1992 


with ESR 


330 healthy 


1988- 


Dic+cr 


15-fold 


Domracheva 




adults 


1990 


Tralo, 
FISH 


6.5-fold 


et al. 2000 




46 patients 


1988- 


Dic+cr 


(6-18)-fold 


Domracheva 




with hematol. 
malignancies 


1990 


Tralo, 
FISH 


(6.5-16)-fold 


et al. 2000 




35 adults 


1990 


Die 


circ 30-fold*) 

overdispersion; 

2 multiaberrant 
cells 


Verschaeve et 
al. 1993 




36 children 


1994 


Die 


(3.2-8)-fold 


Barale et al. 
1998 




20 children 


1996 


Tralo, 


3-fold 


Scarpato et al. 


Controls from 






FISH 


significant 


1997 


Pisa 


70 children 


1996 


Dic+cr 


18-fold 


Gemignani et 
al. 1999 


1 years after 
the accident ! ! 



*) Estimation by the writers 



75 



Table 5. 3 Biological dosimetry in highly contaminated regions > 37 kBq/m 2 



Die dicentric chromosomes, cr centric rings 



Region 


137 Cs 
kBq/m 2 


Sample 


Date of 
investiga- 
tion 


Method 


Results 

Mean elevation 

& specialities 


Authors 


Remarks 


Ukraine/Lugyny district 




130 children 


1988-1990 


Dic+cr 


Increase to 6.6-fold 


Eliseeva et al. 


Effect not explainabL 


Malahovka 










in 1990 


1994 




Russia/Kaluga region 
















Mladenik 


140 


17 adults 


1989 


Dic+cr 


circ 5-fold*) 


Bochkov et al. 




Ogor 


43 


16 adults 






circ 2-fold*) 


1991 




Russia/Bryansk region 
















Clynka 


633 


61 adults 


1989-1998 


Dic+cr 


7-fold 


Sevan 'kaev 


2 multiaberrant cells 


Yordevka 


444 


432 adults 






1.5-fold 


2000 




Klincy 


230 


170 adults 






2-fold 






Russia/Kaluga region 
















Uljanovo 


140 


666 adults 






4-fold 




27 multiaberrant cells 


Chicdra 


100 


548 adults 






2.5-fold 






Kaluga-Bryansk region 
















Uljanova district 


200 


333 children 


1989-1998 


Dic+cr 


3-fold 


Sevan 'kaev et 


Physical estimates (tc 



ECRR Proceedings Lesvos 2009 



Chicdra district 


100 


& juveniles 

407 children 
& juveniles 


1990-2003 




3.7-fold 
no decline 


al. 2005 


11.4mSvand6.7mS 


Ukraine region 


>550 


6 adults 


1991 


Die 


circ 5-fold*) 


Ganina et al. 
1994 




Bryansk and Bryansk 
region 


>550 


1300 


1992 


unstable; 
stable 


5 % > 400 mSv 
1 % 1000 mSv 


Vorob'ev et al. 
1994 


Physical estimate 17- 
multiaberrant cells 


Bryansk region 
Mirnye 


> 1100 


100 adults 


1993 


cr 


4-fold 

6 multiaberrant 
cells 


Salomaa et al. 
1997 


Controls from Krasm 
< 37 kBq/m 2 (Dies 0, 
multiaberrant cells 2) 



*) Estimation by the writers 



ECRR Proceedings Lesvos 2009 

Biological dosimetry in western parts of Europe 

In Austria and Germany, the Alps regions were predominantly affected by 
Chernobyl fallout which was washed out there by rain falls. Some chromosome 
studies were therefore also carried out in these regions. Pohl-Ruling et al. (1991) 
studied 16 adults of Salzburg city, Austria, in 1987 (June- August). The results for 
dic+cr are given in Table 5.4. The physical dose estimate was derived by the authors 
using UNSCEAR modeling. Two of the citizens had been studied already in 
1984/1985, i.e., before the accident. They were followed up also in 1988 and 1990 
(Fig. 2). 

Stephan and Oestreicher (1993) studied 29 persons in Berchtesgaden, Germany, 
which is only 20 km away from Salzburg. Two areas with low contamination in 
southern Germany, Baden-Baden and Tirschenreuth (near to the Czech frontier), 
were selected for control (Table 4). The physical dose estimates were taken by the 
authors from German authorities. The elevation factors given for the dic+cr rate in 
table 5.4 were derived by us using the former published labor control of the authors 
0.9 10" 3 (Stephan and Oestreicher 1989). 

Both studies in the Alps region lead to elevations of dic+cr which are far above 
the equivalent calculated excess exposures. While the Salzburg investigators found a 
correlation between aberration rate and measured Chernobyl deposition, the German 
investigators doubted the causation by radiation because of the high aberration rates 
in their controls. In contrast to this they found a significant decrease with time in a 
subgroup of the Berchtesgaden sample (Table 4). Further there were several cells 
showing an overdispersion of aberrations and therefore an incorporation of alpha 
radioactivity. 

Norway was contaminated in spots up to 600 kBq/m 2 of Cs 137. Brogger et al. 
(1996) carried out chromosome studies in three such regions and found a 10-fold 
elevation of dic+cr still 5 years after the accident. The doses were calculated based 
on whole body counter measurement of Cs 134 and Cs 137 using dose conversion 
factors of the ICRP. The authors interprete the enormous discrepancy to the 
aberration findings as due to a biphasic dose-response. Salbu et al. (2004) reported 
that radioactive particles from Chernobyl were released predominantly by the fire 
after the explosion which contributed significantly to the population exposure even 
in Norway. They contained fission products but also heavy fuel and breeding 
products as U and Pu. 



78 



ECRR Proceedings Lesvos 2009 

Table 5. 4 Biological dosimetry in persons living in West European regions 
contaminated by Chernobyl releases 



Region 


Sample 


Date 
of 


Results 


Physical 
excess dose 






study 


dic+cr 
overdispersion 


estimate 


Austria 


16 adults 


1987 


6-fold 




0.1-0.5 


Salzburg 










mSv 


Germany 
Berchtesgaden 


27 adults 

and 

2 children 


1987- 
1991 


3-2 
fold 


6 cells with 2 die 


<1.6mSv 


Baden-Baden 


20 adults 


i"> 


3-fold 






Tirschenreuth 


1 1 adults 


i"> 


2-fold 


In 1 person 3 
cells with 2 die 


<0.14mSv 


Berchtesgaden 
Subgroup 


5 

9? 


87/88 
90/91 


3-fold 
1.6- 
fold 


1 multiaberrant 
cell 


<0.14mSv 


Norway, 


44 reindeer 


1991 


10- 




5.5 mSv 


selected 
regions 


sames and 
12 sheep 
farmers 




fold 







79 



ECRR Proceedings Lesvos 2009 



CO 

b 

H 
X 



t 

u 
5 



♦ ; r 

1 1 +- 

; ♦ ; i 

1 1 4 

i i j_ 

-i- i r -f 



984 1985 1986 1987 1988 1989 1990 1991 

Year 



Fig. 5. 2 Mean rate ofdic+cr in 2 citizens of Salzburg 
(Pohl-Ruling et al 1991) 



Discussion 

Some of the cited authors used control cohorts from so-called uncontaminated 
regions, e.g. from Kyiv or Minsk. Persons living there show, however, significant 
elevations compared to background rates in really non-exposed individuals even 
after several years. This can be explained by the consumption of contaminated food. 
To evaluate the real mean exposure of the population such investigations in the 
regions of low surface contamination by Cs-137 would be most informative. They 
are also to find in the literature. It must be mentioned that this present compilation of 
data is preliminary and incomplete. 

Conclusions 

Cytogenetic studies which are suitable to evaluate the dose estimates in regions 
contaminated by Chernobyl fallout were done in some thousand persons. The 
following conclusions can be drawn: 

1. Assuming predominant exposure by external and internal Cs-137 the rate of 
dic+cr allows to estimate a minimum accumulated dose and using FISH to 
estimate the accumulated dose in the highly contaminated regions. 



80 



ECRR Proceedings Lesvos 2009 

Physically estimated dose values can therefore be falsified if being much 
lower. 

2. Clustering of the aberrations in the cells and/or multiaberrant cells are a 
reliable indicator of incorporated alpha activity. This was observed in 
several studies outside the distance of 100 km from the source and means 
that the assumption of UNSCEAR that fuel and breeding products are 
abroad negligible is wrong. 

3. If the rate of the instable die does not or not adequately decline over years, 
which is shown in some of the studies, the exposure can also not be 
generated by predominant Cs-137 contribution because of the short 
biological half-life of Cs (circ 100 days), otherwise one had to assume a still 
increasing Cs-contamination in the food. 

4. The dose assumptions of UNSCEAR have to be revised. The physical 
estimates of other authors and the numerous EPR-measurements should be 
also taken into account. 

5. Statements that an observed effect can not be radiation-induced because 
there is no dose-effect relationship should be checked regarding the 
assumptions for dose calculation. A lacking correlation with the ground 
contamination by Cs-137 dose not justify such a conclusion. 



81 



ECRR Proceedings Lesvos 2009 



References 



Barale, R., Gemignami, F., Morizzo, C, Lori, A., Rossi, A., Antonelli, A., Di 
Pretoro, G., Panasuik, G., Ballardin, M.: Cytogenetic damage in lymphocytes of 
healthy andd thyroid tumor-affected children from the Gomel region (Belarus). 
Mutat. Res. 405 (1998) 89-95 

Barcinsky, M.A., Abreu, M.C.A., de Almeida, J.C.C., Naya, J.M., Fonseca, L.G., 
Castro, L.E.: Cytogenetic investigation in a Brazilian population living in an area of 
high natural radioactivity. Am. J. Hum. Genet. 27 (1975) 802-806 

Bezdrobnaia, L.K., Tsyganok, T.V., Romanova, E.P., Tarasenko, L.V., 
Fedorchenko, V.I.: Dynamic study of the cytogenetic effects in blood lymphocytes 
from humans living in the Chernobyl Atomic Energy Station exclusion zone without 
permission. Radiats. Biol. Radioecol. 42 (2002) 727-30 (in Russian) 

Bochkov, N.P., Katosova, L.D., Sapacheva, V.A., Platonova, V.I., Smirnova, 
T.D., Pitkevich, V.A.: Cytogenetic analysis of the peripheral blood lymphocytes in 
people residing in regions of the Kaluga Oblast polluted with radionuclides. Med. 
Radiol. (Mosk.) 36 (1991) 50-52 (in Russian) 

Bochkov, N.P., Katosova, L.D.: Analysis of multiaberrant cells in lymphocytes 
of persons living in different ecological regions. Mutat. Res. 323 (1994) 7-10 

Brogger, A., Reitan, J.B., Strand, P., Amundsen, I.: Chromosome analysis of 
peripheral lymphocytes from persons exposed to radioactive fallout in Norway from 
the Chernobyl accident. Mutat. Res. 361 (1996) 73-79 

Domracheva, E.V., Aseeva, E.A., Obukhova, T.N., Kobzev, Y.N., Olshanskaya, 
Y.V., Dyachenko, L.V., Udovichenko, A.I., Zakharova, A.V., Milyutina, G.I., 
Nechai, V.V., Vorobiov, A.I.: Cytogenetic features of leukaemias diagnosed in 
residents of areas contaminated after the Chernobyl nuclear accident. Appl. Radiat. 
Is. 53(2000)1171-1177 

Eliseeva, E., Iofa, E.L., Stoian, E.F., Shevchenko, V.A.: An analysis of 
chromosome aberrations and SCE in children from radiaiton-contaminated regions 
of Ukraine. Radiats. Biol. Radioecol. 34 (1994) 163-171 (in Russian) 

Feshchenko, S.P., Schroder, H.C., Miiller, W.E.G., Lazjuk, G.I.: Congenital 
malformations among newborns and developmental abnormalities among human 
embryos in Belarus after Chernobyl accident. Cell. Mol. Biol. 48 (2002) 423-426 



82 



ECRR Proceedings Lesvos 2009 



th 



Fritz-Niggli, H. (1997) Strahlengefahrdung/Strahlenschutz, 4 m ed., Hans Huber, 
Bern, Switzerland 

Ganina, K.P., Polischuk, L.Z., Buchinskaya, L.G., Nesina, LP., KindzeLskii, 
Demina, E.A., Usatenko, V.D., Chebotareva, E.D., Yakimova, T.P., Maznik, N.A., 
Nikiforova, N.A.: Cytogenetic investigation in individuals exposed to radiation in 
some regions of Ukraine. Tsitologiya i Genetika 28 (3) (1994) 32-37 

Gemignani, F., Ballardin, M., Maggiani, F., Rossi, A.M., Antonelli, A., Barale, 
R.: Chromosome aberrations in lymphocytes and clastogenic factors in plasma 
detected in Belarus children 10 years after Chernobyl accident. Mutat. Res. 446 
(1999)245-253 

Hoffmann, W., Schmitz-Feuerhake, I.: How radiation-specific is the dicentric 
assay? J. Exp. Analysis Environ.Epidemiol.2( 1999)1 13-33 

Jiang, T., Hayata, I., Wang, C, Nakai, S., Yao, S., Yuan, Y., Dai, L., Liu, Q., 
Chen, D., Wei, L., Sugahara, T.: Dose-effect relationship of dicentric and ring 
chromosomes in lymphocytes of individuals living in the high background radiation 
areas in China. J. Radiat. Res. 41, Suppl. (2000) 63-68 

Imanaka, T., Koide, H.: Assessment of external dose to inhabitants evacuated 
from the 30-km zone soon after the Chernobyl accident. Radiats. Biol. Radioecol. 40 
(2000) 583-589 

Maznik, N.A., Vinnikov, V.A., Lloyd, D.C., Edwards, A. A.: Chromosomal 
dosimetry for some groups of evacuees from Prypiat and Ukraine liquidators at 
Chernobyl. Radiat. Prot. Dos. 74, Nos. 1/2 (1997) 5-11 

Maznik, N.A.: Long-term follow-up cytogenetic survey and biological dosimetry 
in persons evacuated from 30-km Chernobyl zone. Radiats. Biol. Radioecol. 44(5) 
(2004) 566-573 (in Russian) 

Mikhalevich, I.S., Lloyd, D.C., Edwards, A. A., Perepetskaya, G.A., Kartel, N.A.: 
Dose estimates made by dicentric analysis for some Belarussian children irradiated 
by the Chernobyl accident. Radiat. Prot. Dos. 87, No.2 (2000) 109-1 14 

Padovani, L., Caporossi, D., Tedeschi, B., Vernole, P., Nicoletti, B., Mauro, F.: 
Cytogenetic study in lymphocytes from children exposed to ionizing radiation after 
the Chernobyl accident. Mutat. Res. 319 (1993) 55-60 



83 



ECRR Proceedings Lesvos 2009 

Pilinskaia, M.A., Dybskii, S.S., RecTko, D.V.: The cytogenetic effect in a group 
of settlers from a 30-kilomter area of right of way. Tsitol. Genet. 33(6) (1999) 39-44 
(in Russian) 

Pohl-Riiling, J., Haas, O., Brogger, A., Obe, G., Lettner, H., Daschil, F., 
Atzmiiller, C, Lloyd, D., Kubiak, R., Natarajan, A.T.: The effect on lymphocyte 
chromosomes of additional burden due to fallout in Salzburg (Austria) from the 
Chernobyl accident. Mutat. Res. 262 (1991) 209-217 

Prohl, G., Muck, K., Likhtarev, Kovgan, L., Golikov, V.: Reconstruction of the 
ingestion dose received by the population evacuated from the settlements in the 30- 
km zone around the Chernobyl reactor. Health Physics 82 (2002) 173-181 

Salbu, B., Lind, O.C., Skipperud, L.: Radionuclide speciation and its relevance in 
environmental impact assessments- J. Environ. Radioactivity 74 (2004) 233-242 

Salomaa, S., Sevan'kaev, A.V., Zhloba, A.A., Kumpusalo, E., Makinen, S., 
Lindholm, C, Kumpusalo, L., Kolmakow, S., Nissinen, N.: Unstable and stable 
chromosomal aberrations in lymphocytes of people exposed to Chernobyl fallout in 
Bryansk, Russia. Int. J. Radiat. Biol. 71 (1997) 51-59 

Scarpato, R., Lori, A., Panasiuk, G., Barale, R.: FISH analysis of translocations 
in lymphocytes of children exposed to the Chernobyl fallout: preferential 
involvement of chromosome 10. Cytogenet. Cell Genet. 79 (1997) 153-156 

Scheid, W., Weber, J., Petrenko, S., Traut, H.: Chromosome aberrations in 
human lymphocytes apparently induced by Chernobyl fallout. Health Phys. 64 
(1993)531-534 

Serezchenko, V.A., Domracheva, E.V., Klezeval, G.A., Kulikov, S.A., 
Kuznetzov, S.A., Mordvintcev, P.I., Sukhovskaya, L.I., Schlokovsky-Kordi, N.E., 
Vanin, A.F., Voevodskaya, N.V., Vorobiev, A.I.: Radiation dosimetry for residents 
of the Chernobyl region: a comparison of cytogenetic and electron spin resonance 
methods. Radiat. Prot. Dosi. 42, No.l (1992) 33-36 

Sevan 'kaev, A.V., Tsyb, A.F., Lloyd, D.C., Zhloba, A.A., Moiseenko, V.V., 
Skrjabin, A.M., Climov, V.M.: 'Rogue'cells observed in children exposed to 
radiation from the Chernobyl accident. Int. J. Radiat. Biol. 63 (1993) 361-367 

Sevan 'kaev, A.V.: Results of cytogenetic studies of the consequences of the 
Chernobyl accident. Radiats. Biol. Radioecol. 40(5) (2000) 589-595 (in Russian) 



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ECRR Proceedings Lesvos 2009 

Sevan 'kaev, A.V., Mikhailova, G.F., Potetnia, O.I., Tsepenko, V.V., 
Khvostunov, I.K., Golub, E.V., Piatenkko V.S., Pozdyshkina, O.V., ShepeF, N.N., 
Matveenko, E.G.: Results of dynamic cytogenetic study of children and teenagers 
living in areas radioactive by contamination after the Chernobyl accident. Radiats. 
Biol. Radioecol. 45(1) (2005): 5-15 (in Russian) 

Stephan, G., Oestreicher, U.: An increased frequency of structural chromosome 
aberrations in persons present in the vicinity of Chernobyl during and after the 
reactor accident. Is this effect caused by radiation exposure? Mutat. Res. 223 (1989) 

7-12 

Stephan, G., Oestreicher, U.: Chromosome investigation of individuals living in 
areas of southern Germany contaminated by fallout from the Chernobyl reactor 
accident. Mutat. Res. 319 (1993) 189-196 

UN Chernobyl Forum Expert Group "Health" (EGH). Health Effects of the 
Chernobyl Accident and Special Health Care Programmes. Geneva: World Health 
Organisation 2005 

Verschaeve, L., Domracheva, E.V., Kuznetsov, S.A., Nechai, V.V.: Chromosome 
aberrations in inhabitants of Byelorussia: consequence of the Chernobyl accident. 
Mutat. Res. 287 (1993) 253-259 

DeVita, R., Olivieri, A., Spinelli, A., Grollino, M.G., Padovani, L., Tarroni, G., 
Cozza, R., Sorcini, M., Pennelli, P., Casparrini, G., Crescenzi, G.S., Mauro, F., 
Carta, S.: Health status and internal radiocontamination assessment in children 
exposed to the fallout of the Chernobyl accident. Arch. Environ. Health 55 (2000) 
181-186 

Vorob'ev, A.I., Domracheva, E.V., KlevezaF, G.A., Meshcheriakov, L.M., 
Moiseeva, T.N., Osechinskii, I.V., Serezhenkov, V.A., Shklovskii-Kordi, N.E.: 
Cumulative radiation dosage and epidemiological research in the Chernobyl region. 
TerArkh. 66(7) (1994) 3-7 



85 



ECRR Proceedings Lesvos 2009 



Cancer risks of low dose ionising radiation 



Prof. Roza Goronchova 

Institute of Genetics, National Academy of Sciences, Belarus 

I will start by discussing the characteristics of the Life Span Study Cohort (LSS) in 
Japan. Survivors with dose estimates in excess of lGy comprise less than 3% of the 
cohort. Of the 105,000 members of the LSS included in the current analysis, about 
35,000 received doses between 5 and 200 mGy. In fact, they comprise about 75% of 
the cohort members with dose above 5 mGy (Preston et al 2007) 

The mean dose in the LSS cohort was 200mSv (Preston et al 2003). 



LOW-DOSE RADIATION RISKS 



15 



1.4 



* 1,3 

s 
s 

% 

M 1-2 

CO 



1.1 



1.0- 




0.0 



0.1 



0.2 



— i— 
0.3 



0.4 



i 
0.5 



Gamma-Ray Dose Equivalent (Sv) 



Figure 6.1 - Radiation related cancer risks at low doses among atomic bomb 
survivors 



86 



ECRR Proceedings Lesvos 2009 



In Fig 6.1 we can see age-specific cancer rates over the 1958-1994 follow-up period 
relative to those for an unexposed person, averaged over the follow-up and over sex, 
and for age at exposure 30. The dashed curves represent ±1 standard error for the 
smoothed curve. The straight line is the linear risk estimate computed from the range 
0-2 Sv. Because of an apparent distinction between distal and proximal zero-dose 
cancer rates, the unity baseline corresponds to zero-dose survivors within 3 km of 
the bombs. The horizontal dotted line represents the alternative baseline if the distal 
survivors were not omitted. The inset shows the same information for the fuller dose 
range (Pierce and Preston 2000) 

Analyses of these data sets based on more than 40 years of cancer incidence 
data for the members of the LSS were made. Thirty four percent of the cancers 
included in the current analyses were diagnosed during 1988-1998. There is a 
statistically significant dose response when analyses were limited to cohort members 
with doses of 0.15 Gy or less (Preston et al 2007) 



Region 


Collective dose 

for children and adolescents 

(0—18 at the time 

of the accident). 


Collective dose 

for adults (19 years 

and older at the time 

of the accident). 


Total collective doses 

of Belarusian population, 

person-Gy 




person -Gy 


person-Gy 




Brest 


21129 


24042 


45171 


Vitebsk 


1164 


1560 


2724 


Gomel city 


36998 


38236 


75234 


Gomel 


112812 


171939 


284751 


Grodno 


3329 


4453 


7782 


Minsk city 


15063 


19244 


34307 


Minsk 


6404 


8121 


14525 


Mogilev 


22328 


27694 


50022 



Figure 6.2 - Collective thyroid doses for two age groups in Belarus: [20 Years after 
the Chernobyl Catastrophe: the consequences in the Republic of Belarus and their 
overcoming. (National Report, 2006)] 



87 



ECRR Proceedings Lesvos 2009 







7 - 


u- la years om ■ ■ 


Total (1986-2001): 


6 


" at the moment of accident - 


1635 cases 


5 


1 1 1 1 1 1 1 ' 




j - 


i 1 1 1 1 1 1 1 1 1 


Control for <I 8 years aid 


3 " 


■ 1 p 


(wr-ms): 


7 


m 
m — — — . — — — - 


14 cases 


1 - 




(I case /I min persons /year) 


L' 


19SA 1937 19RS I9J39 19?0 IM1 1992 1193 1994 1995 1996 1??7 )??$ W?2ffl»2W>l 


| 








12- 


> 18 years old 1 
at tli e inntTifiit of accident _ ■ 1 


Total (1986-2001): 


10 - 




6460 cases 








6 - 






4 - 


■ 1 


Control for ^18 years otd 
(T973-I985): 






1393 cases 



19B6 19B7 198S 1989 1990 1991 1992 1193 1994 T99S 1996 1997 1998 1999 2000 2001 



Figure 6.3 -In cases per hundred persons, the time course of thyroid cancer 
incidence in Belarus (National Report, 2003) 



J imc period 


Collective effective dose, | 


jeuson-Sv 




external 


internal 


cumulative 


1986-1995 
1986-2005 


9636 
11900 


5504 
6800 


15140 
18700 



Figure 6.4 - Collective cumulative effective doses (excluding thyroid doses) for two 

time periods for territories of Belarus with density of cesium- 137 contamination 

over 37 kBq/m2[20 Years after the Chernobyl Catastrophe: 

the consequences in the Republic of Belarus and their overcoming. 

National Report, 2006] 



88 



ECRR Proceedings Lesvos 2009 



Tumor site 


ICDX 

code 


Male 


Female 


GPR5 


Control 


GPR5 


Control 


Total 


C00-97 


542.95* 


487.21 


359.12* 


301.89 


Stomach 


C16 


69.55 


65.75 


29.33 


28.22 


Colon 


C18 


23.31* 


17.94 


16.41 


15.43 


Lungs 


C34 


115.91 


121.16 


8.56 


8.81 


Skin 


C44 


57.56* 


39.82 


47.27* 


32.96 


Breast 


C50 






72.29* 


59.25 


Kidney 


C64-65 


19.9 


20.71 


9.26 


9.37 


Bladder 


C67 


26.38 


24.61 


3.37* 


2.69 


Thyroid 
gland 


C73 


6.54* 


2.58 


22.08* 


16.63 



Figure 6.5 - Standardized incidence rate of malignant tumors among the population 
living on the territories of Belarus with 37-555 kBq/m and in the control group 
for the period of 1993-2003 (per 100 000 populations) [Okeanov A.EJ/Zum int. 
Kongress "20 Jahre Leben mit Tschernobyl, 2006] 



89 



ECRR Proceedings Lesvos 2009 



Tumor site 


ICDX 

code 


1993-1996 


1997-2003 


RR 


95% CI 


RR 


95% CI 


Total 


C00-97 


1.09 


1.07-1.12 


1.15 


1.13-1.17 


Stomach 


C16 


1.03 


0.97-1.09 


1.03 


0.96-1.07 


Colon 


C18 


1.01 


0.91-1.12 


1.23 


1.15-1.32 


Lungs 


C34 


0.91 


0.86-0.97 


0.93 


0.89-0.98 


Skin 


C44 


1.26 


1.18-1.35 


1.48 


1.42-1.54 


Breast 


C50 


1.16 


1.08-1.26 


1.25 


1.18-1.32 


Kidney 


C64-65 


1.04 


0.91-1.18 


0.94 


0.86-1.02 


Bladder 


C67 


1.05 


0.93-1.19 


1.05 


0.97-1.15 


Thyroid 
gland 


C73 


1.45 


1.23-1.71 


1.46 


1.33-1.59 



Figure 6.6 - Relative risk of malignant tumors incidence among the population 
living on the territories of Belarus with 37-555 kBq/m [Okeanov A.EJ/Zum int. 
Kongress "20 Jahre Leben mit Tschernobyl, 2006] 



90 



ECRR Proceedings Lesvos 2009 




n 1 1 1 1 1 1 1 

0,DO 0,02 0,04 0,06 0,03 0,10 0,12 0,14 0.1B 

Accumulated dose, Sv 



Figure 6.7 - Dose dependence of breast cancer incidence in women of Gomel 
region, Belarus [20 Years after the Chernobyl Catastrophe: the consequences in the 
Republic of Belarus and their overcoming. National Report, 2006] 

Now if we recall Figure 6. 8, the radiation-related cancer risks at low doses among 
atomic bomb survivors we can compare the populations. 



91 



ECRR Proceedings Lesvos 2009 



Dose category 


ERR 


ERR per Sv 


0.005-0.02 


0.03 


2.6 ±2.1 


0.02-0.05 


0.05 


1.6 ±0.90 


0.05-0.10 


0.04 


0.60 ± 0.40 


0.10-0.20 


0.06 


0.43 ± 0.25 


0.20-0.50 


0.12 


0.38 ±0.13 



Figure 6.8 - Studies of the mortality of atomic bomb survivors. Report 12, Parti. 
Cancer: 1950-1990 [D.A. Pierce, Y. Shimizu, D.L. Preston, M. Vaeth, K. Mabuchi // 
Radiation Research, 1996] 

Inverse dose-rate effects 



CD 
CD 



O 
Q_ 




y= 0J55x + 1 973 
R 2 = 1578 



: 5 1 1,5 2 2 f 5 

Whole-body a bsarbed dose of chronic irraciation,cGy 

Figure 6.9 -Relationship between the MN-PCE frequency in bone marrow and 
lifetime whole-body absorbed dose in bank voles at site 2 (x) and site 4 (o) 



92 



ECRR Proceedings Lesvos 2009 





14 




12 


CO 


10 


<x> 




o 




o 


8 


<z> 




o 








LU 


6 


O 




n 




-^ 


4 



y= 0.09x ->^34° 
R2 =^99"* 



y = 0,00035x2 + 0,06505x + 2,40810 
R2 = 0,9975** 







20 



40 



60 



80 



100 



Absorbed dose of acute gamma-irradiation, 
cGy 



Figure 6.10 - Relationship between the MN-PCE frequency in bone marrow and 
absorbed dose of acute gamma-irradiation in animals at site 2 (x) and site 4 (o) 



Employer/site 


Dose range, mSv 


Total no. 

of workers 


Collective 

dose, 
person Sv 


Mean 
dose, 
mSv 


<10.0 


10.0-50.0 


50.0-100.0 


100.0+ 


Atomic Weapons Establishment 


10.778 


1.053 


174 


139 


12.144 


76 


6.2 


British Nuclear Fuels pic 


12.057 


8.621 


3.334 


5.233 


29,245 


1.936 


66.2 


Industrial* 


1.931 


603 


120 


76 


2.730 


48 


17.6 


Ministry of Defence 


26.282 


5.169 


1.102 


931 


33.484 


418 


12.5 


Nuclear Electric and Magnox 
Generation 


5.718 


4.153 


954 


586 


11.411 


275 


24.0 


Nycomed Amersham 


2.096 


594 


171 


285 


3.146 


118 


37.4 


Research b 


1.944 


696 


100 


46 


2.836 


36 


12.7 


Scottish Nuclear 


1.374 


693 


327 


189 


2.583 


71 


27.8 


United Kingdom Atomic Energy 
Authority 


16.271 


6.824 


1.974 


2.095 


27.164 


832 


30.7 


Total 


78.501 


28.406 


8.256 


9.580 


124,743 


3.810 


30.5 



a Industrial: Rolls-Royce and Associates, plus non-destructive testing firms. 

b Research: Council for the Central Laboratory of the Research Councils, MRC Radiobiology Unit and NRPB. 

Figure 6.11 - Study population for the second analysis of the National Registry for 
Radiation Workers (NRRW) by lifetime dose and first employer [Muirhead C.R., 
O'Hagan J. A., Kendall G.M. // Radiat Biol. Radioecol, 2008] 



93 



ECRR Proceedings Lesvos 2009 



Analysis 


Leukaemia 

excluding CLL 


All malignant neo- 
plasms excluding 
leukaemia 


All malignant neo- 
plasms excl. leu- 
kaemia and lung 
cancer 


2nd NRRW analysis (Muirhead et al„ 1999) 

1st NRRW analysis (Kendall et al., 1992) 

IARC International Study (Cardis et al., 2005, 2007) 

Japanese A-bomb survivors (Pierce et al., 1996) 


2.55 (-0.03, 7.16) 
4.28 (0.40, 13.6) 
1.93 (<0, 7.14) 
2.15(0.43,4.68) 


0.09 (-0.28, 0.52) 
0.41 (-0.17, 1.15) 
0.97(0.27,1.80) 
0.24(0.12,0.37) 


0.17 (-0.26, 0.70) 
0.56 (-0.14, 1.48) 
0.59 (-0.16, 1.51) 
0.19(0.07,0.33) 



Figure 6.12 - Estimates of excess relative risk (ERR) per Sv (and 90% CI) in the 
NRRW, the IARC study and the Japanese A-bomb survivors [Muirhead C.R., 
O'Hagan J. A., Kendall G.M. // Radiat Biol. Radioecol, 2008] 

Conclusions 

Doses of the whole body irradiation of affected populations of the Republic of 
Belarus, Ukraine and contaminated regions of the Russian Federation are in the dose 
range of 0-0.15 Gy, i. e. within the range of doses that caused statistically reliable 
increase in cancer incidence in atomic bomb survivors. Thyroid cancer incidence 
increases steadily among adult population of Belarus (National report, 2006). 

A statistically significant increase of the breast cancer incidence among 
women of Gomel region in comparison with appropriate value among women living 
in the less contaminated areas was observed in the period 1990-2003. Dose 
dependence between accumulated radiation dose and realized relative risk of breast 
cancer was shown (National report, 2006). According data of A. Okeanov 
population living in regions with contamination levels of 37-555 kBq/m2 
demonstrated considerable growth of the incidence in cancers in 1997-2003 in 
comparison with the previous period 1993-1996. We suppose that an increased 
thyroid cancer incidence in children born by irradiated parents chronically exposed 
due to the Chernobyl accident can be resulted from a induced genomic instability 
(Goncharova, 2005). There is an increasing set of data showing that radiation risks 
of chronic irradiation of populations at low doses and low dose rates are higher than 
radiation risks of atomic bomb survivors. The 15-country collaborative study of 
cancer risk among radiation workers of the nuclear industry give evidence that 
excess relative risks (ERR) of all malignant neoplasm excluding leukaemia and lung 
cancer is approximately 3 times higher than radiation risk of atomic bomb 
survivors. This means that using of radiation risks established for atomic bomb 
survivors and Dose and Dose Rate Effectiveness Factor (DDREF) higher than 1 in 
case of chronically irradiated populations will underestimate numbers of radiation- 
induced cancers. Thus any declarations about an absence of radiation-induced 
increases in the incidence of solid cancers excluding thyroid cancer simply mean an 
ignoring of data established in Belarus. It is clear that conclusions of the UN 
Chernobyl Forum report have no scientific base and are therefore misleading. 



94 



ECRR Proceedings Lesvos 2009 

7 
Nanoparticles and Radiation 

Andreas Elsaessar, Chris Busby, George McKerr, C. Vyvyan Howard 

Centre for Molecular Biosciences, University of Ulster 

(These results were originally given as a poster: Elsaesser A, Busby C, McKerr G 
and Howard CV (2007) Nanoparticles and radiation. EMBO Conference: 
Nanoparticles. October 2007 Madrid and also: Elsaesser A, Howard C. V., & Busby 
C. (2009) The biological implications of radiation induced photoelectron production, 
as a function of particle size and composition. International Conference; Royal 
Society for Chemistry NanoParticles Liverpool 2009) 

Interaction of Radiation and Matter 

Electromagnetic radiation and matter interact predominantly by three different 
mechanisms: Compton scattering, the photoelectric effect and pair production. 
Compton scattering basically describes the loss of incident photon energy by the 
scattering of shell electrons. Pair production is the simultaneous production of an 
electron and a positron and occurs at energies above 1.022MeV, which is equivalent 
to the invariant mass of an electron plus positron. With the photoelectric effect 
electrons absorb the incident photon energy and are either emitted or lose energy in 
secondary processes. For energies below lMeV the photoelectric effect is the 
predominant one. The cross section a for the photoelectric effect is proportional to 
Z (atomic number) to the power 5 and roughly proportional to the incident photon 
energy to the power -7/2. 

<i = Z 5 E T - 7/2 

Most of the photoelectrons produced in an absorbing material lose their energy 
though electron-electron scattering and Bremsstrahlung (breaking radiation). 
Therefore the escape depth of photoelectrons generated in solids is usually a few 
nanometers [1]. 

Hence, irradiated particles with diameters in the range of a few nanometres 
will emit most of the generated photoelectrons without internal absorption. 
Therefore nanoparticles are likely to emit the largest quantity or secondary electrons 
in proportion to their mass. Furthermore, secondary electron emission of high Z 



95 



ECRR Proceedings Lesvos 2009 

materials could provide a partial explanation of the toxicity of various heavy metals. 
Due to their size, nanoparticles can penetrate into the human body and some are able 
to reach the cell nucleus. This may be crucial; in explaining the toxicity of 
incorporated nanoparticles of materials with a high atomic number [2,3]. 




Fig 7.1 Beam and target geometry 



96 



ECRR Proceedings Lesvos 2009 



*^ 10 * 



Ffg2a 



i 



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water **»."* 

_. 100.000 primary photon* 




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Fig 7.2 Secondary electron production by WOkeV primary photons within the target and escaping electrons overlay ed by the target 
geometry for water (a), gold (b) and Uranium (c). Fig 2 d-f (lower) shows the corresponding energy deposition. Note that these are 
projections in two dimensions: tracks out of the plane of the paper are not shown. For water the scale is 100 times greater i.e. 
100,000 photons produce the 4 tracks compared with 1000 photons producing the tracks shown in the Uranium and Gold case. 



97 



ECRR Proceedings Lesvos 2009 



Monte Carlo Simulations 

Monte Carlo simulations are widely used in computational and statistical physics, 
physical chemistry and high energy physics to model particle transport and particle 
matter interactions. We employed FLUKA [4,5] a Monte Carlo code to simulate the 
interaction and propagation or photons and photoelectrons in matter composed of 
different particles. FLUKA is capable of simulating particle interactions from IkeV 
to TeV for different hadrons, leptons and bosons with high accuracy. We modelled 
photon absorption and secondary electron production of particles from 1cm to a 
Angstrom for incident photon energies in the keV region. Target materials we used 
were water (Z eff = 7.5), Gold (Z=79) and Uranium (Z=92). Fig 1 shows the 
arrangement of photon beam and target. Fig 2 shows secondary electron production 
and energy deposition. Fig 3 illustrates the ratio of secondary electromn production 
to primary incident photons and Fig 4 shows the same ratio but weighted with the 
beam projection area and the target volume. 




<^ ^ target raUus (gold) 



Fig 7.3 Ratio of electrons leaving the target material (gold) to incident primary 
photons (lOOkev, WkeV and 2 keV) 



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ECRR Proceedings Lesvos 2009 



Conclusion 



Secondary electron emission from lnm nanoparticles is about 25000 times higher 
than from the equivalent particle of 1cm radius. At target sizes of about lOnm the 
emission reaches a plateau with no further increase for smaller targets. This is 
probably due to the negligible internal absorption within the target material and 
hence the increases yield of secondary electrons leaving the nanoparticle. This size 
effect shows an energy dependent maximum for the ratio of generated electrons to 
incident primary photons which shifts for lower photon energies to smaller target 
diameters. The simulations also show an increase in secondary electrons and energy 
deposition within high Z target materials compared to a water phantom. It also 
confirms the energy dependence of secondary electron production as expected by 
the photoelectric cross section. 





^ *F W ^ J^ ^ S tirprtra^mteoldj 



Fig 4. Same ratio as Fig 3 but weighted with the perpendicular beam projection 
area and the target volume. 



99 



ECRR Proceedings Lesvos 2009 



References 



1. Huefner S (1996) Photoelectron Spectroscopy Principles and Applications. 
Berlin: Springer 

2. Busby C (2005) Does Uranium contamination amplify natural background 
radiation dose to the DNA? Eur.J.Biol.Biolmagn. 1(2) 120-131 

3. Hainfeld JF et al (2004) The use of gold nanoparticles to enhance radiation 
therapy in mice. Phys Med Biol 49 N309-N315 

4. Fasso A, Ferrari A., Ranft J, Sala PR (2205) FLUKA: a multi particle rtransport 
code, CERN 2005-19 INFN/TC05/1 1, SLAC-R-773 

5. Fasso A, Ferrari A, Roesler S, Sala PR, Battistoni G, Cerutti F, Gadoiu E, Garzelli 
MV, Balarini F, Ottolenghi A, Empl A and ranft J (2003) The physics models of 
FLUKA: status and recent developments. Computing and high energy physics 
conference Chep 2003, La Jolla, CA March 24-28 2003 (aper MOMT005) ECONF 
C 0303241 2003, ARXIV:HEO-PH/030062 



100 



ECRR Proceedings Lesvos 2009 

8 

Childhood cancer near German nuclear power plants: The 
KiKK study 



Sebastian Pflugbeil and Alfred Korblein 

Munich Environmental Institute, German Society for Radiological Protection, Berlin 

The KiKK study is an epidemiologic study of childhood cancers near German 
nuclear power plants. It was commissioned by the Federal Office for Radiation 
Protection (Bundesamt fur Strahlenschutz), and conducted by German Childhood 
Cancer Registry (GCCR) between April 2003 and December 2007. It comprised an 
external advisory expert commission of 12 people, and after the results were 
published in an American scientific journal in 1999, the wide media coverage forced 
the German Federal Office of Radiation Protection to take action. In 2001 it 
commissioned a new study which was meant to investigate the causes for possible 
increased cancer rates near NPPs. The study design differed from a purely 
ecological study - the distance from the plant was included as a proxy of the 
radiation exposure[l]. 



The design of the study follows: 

• Case-control study (3 controls per case, 
matched by age, sex and reactor site) 

• All cancers, sub group: leukaemias 

• All German commercial NPPs 

• Children below age < 5 

• Longest possible study period (1980-2003) 

• One-tailed statistical test 
Proxy of radiation exposure: 
Inverse distance of place of residence at diagnosis 
Main question: 

Increase of cancer rates with decreasing distance from NPP? 
Additional test: 

Cancer rate greater for r < 5 km than for r > 5 km? 
Cancer rate greater for r < 10 km than for r > 10 km? 
Linear logistic regression model: 



• 



101 



ECRR Proceedings Lesvos 2009 

• In(odds) =fi0+fil/r 
where 

odds = cases / controls 

r = distance from NPP; x = 1/r 

jiO, fil : parameters (fil: trend parameter) 

• Negative distance trend if parameter^/ >0 (HO <= 0) 

• The relative risk is the ratio of two odds: 

RR = odds(x)/odds(x=0) = exp(ftO+fil *x)/exp(ft0) = exp(fil *x) 




Q 30 100 



Figure 8.1 - Study region: countries (3) next to reactor sites (16) - collectively 41 
counties 



102 



ECRR Proceedings Lesvos 2009 



Diagnosis 


Bi±SE 


90% CI 


P value 


cases 


controls 


cancer 


1.18 ±0.44 


0.46, 1.90 


0.0034 


1592 


4735 


leukaemia 


1.75 ±0.67 


0.65,2.85 


0.0044 


593 


1766 



Figure 8. 2 - Results of the study 

We discovered the following: 

Significant negative distance trend for all cancers (p=0.0034) as well as for 
leukaemia (p=0.0044) 

Relative risk for r < 5 km vs. r > 5 km is 

RR=1.61 for all cancers and RR=2.19for leukaemia 

Relative risk for r < 10 km vs. r > 10 km is 
RR=1.18 for all cancers and RR=1.33for leukaemia 

• Significant excess in the 5-km zone'. 

29 excess cancer cases, 20 excess leukaemia cases 

• Negative distance trend also significant when NPP Kriimmel - with known 
leukaemia cluster - is excluded 



103 



ECRR Proceedings Lesvos 2009 



-> -> 




i i i i i i 



5 10 15 20 25 30 35 40 45 50 55 60 65 
djrtmice from NPP I 



n-mr tnrv n xt*>ttt t jx x 



Figure 8.3 - Cancer risk (study region) 



3 



2.5 



2.0 



Si 



1.5 



1.0 - 



5 




5 10 15 

distance from NPP [km] 



— i — 
20 



■i=y$r 



25 



Figure 8.4 - Cancer risk (r < 25km) 



104 



ECRR Proceedings Lesvos 2009 



2.5 



2.0 



§1.5 



1.0 ■- 



0.5 




RR-1/r 2 



i — 



10 20 30 40 50 60 

dtftmite froniNPF I 



80 



nmitnr^ n. TTrti 



Figure 8.5 - Leukaemia risk (Study region) 

The second part of the study comprised a questionnaire. A sub-group (360 cases, 
696 controls) with selected diagnoses (leukaemia, lymphoma, and ZNS tumours) 
were interviewed with regard to the presence of known risk factors for leukaemia 
between 1993 and 2003. None of the risk factors (confounders) had an appreciable 
influence on the distance trend, ie the main result - a negative distance trend - could 
not be explained by confounders. However, we must recognise the low power of the 
study due to the small sample size. 

KiKK Conclusions 

The KiKK study indicated a ignificantly increased cancer risk, mainly for 
leukaemia, when living in the proximity (r < 5 km) of German NPPs. The results 
were crucially not consistent with most international studies, and 'unexpected' given 
the level of radiation exposure. 

The conclusions made were that the causes were unknown, but that radiation 
could be ruled out on principle. Thus the findings are this unexplained. Could there 
be Confounding? Could it be a chance result? 



105 



ECRR Proceedings Lesvos 2009 



Inconsistencies 



A meta-analysis by Baker et al. (2007), explored a pooled analysis of 37 studies 
from 9 countries (136 nuclear facilities). It yielded a demonstrably significant 
increase of leukaemia in children below age 10. New findings of the effects of 
radiation at very low doses point to higher risks from internal emitters (eg genomic 
instability, bystander effect). 



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Figure 8. 6- Baker et al. 2007 results 
The inconsistency is more clear if we compare - 
• Baker and Hoel 2007 



Increase of leukaemia incidence in the 15-km-radius: 
children and young adults < 26 y: 11% 



children 



< 10y: 



23% 



KiKK 

in the 10 km radius: 
children 



< 5y: 



33% 



106 



ECRR Proceedings Lesvos 2009 

KiKK found that leukaemia risks were -doubled (RR=2.19) in children below age 5 
near NNPs. Doubling the dose for childhood leukaemia is a few mSv after in utero 
exposure (from OSCC data). Official German dose estimates for 1 year old children 
are a few |uSv per year (see: 

http://dip21.bundestag.de/dip21/btd/16/068/1606835.pdf). The difference is clear - 
by a factor of 1000! 



Abbildung II. 1-1 



Ableitung radioakther Stoffemit tier Fortluft a us Kernkraftwerken im Jahr 2006 
Sch w eb stoffe u nd J od- 1 3 1 



1E+08 



1E+07 



1E+0i- 



1E+05 



1E+04 



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=\ 








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Figure & J - Releases of "1-131 and particulates from German nuclear plants in 2006 
(Bq). 



107 



ECRR Proceedings Lesvos 2009 



Abbildung II. 1-2 

Ableitung radioaktiver Stoffemit tier Fortluft a us Kemkrafttierken im Jahr 2006 
14 C0 2 , Tritium unci Edelgase 







y 



,r .,# ,? v 



01 Betrieb beendet 



y 



' r 



■+ kk-in-H ■jd'Hi 'iikiJ'i fl.o:hw-^i;:ii^iiZ'f- 



Figure 8.8 - Releases of Tritium, C-14 and radioactive Noble Gases from German 
nuclear plants in 2006 (Bq). 



Deutscher Bundestag - 16. Wahlperiode 



Drucksache 16/6835 



A ti tii mung il i- / 

Stridden exposition im Jabr 2006 in der llingebimg von Kernkrattwerken durcb die 
Ab Lc it img radioaktiver Stoffe mit der Fortluft 



: 01 

0,0 OS 
0,006 
0,004 
0,002 



mSv 



ObererWert a) 
□ effektive Dosis Erwachsene 
(Grenzwert= 0,3 mSv) 
effektive Dosis Klein kinder 
(Grenzwert= 0,3 mSv) 
Schilddrusendosis Kleinkinder 
■ ■:ni^nzvvert= m.iji mSv) 



M 



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> 



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a) Berechnet fiir gins Referenzperson an den ungunstigsten Einwirkungsstellen d* 

b) Die StrahlenexpositJon konnts fur Exposition spfad*. t-^-i clen^n Rodionuklid* in dm V-:-rjjihr^n okkLimulk-rt V/urden. nur 
LinV'Mlj.tiindig l:.*r*d - in*tVrtTd*n. do l:^i di*s*n l^iiikrofr.v-^i-t^n W*rt*fLirdi* £M*itun-;i rodivoktiv-r'-I.tvTfe mit d*r Fvitkift 
aus den Jahren vor 1990 (Greifswald) bzw. vor 1 984 (Rheinsberg) nicht voriiegen 



Figure 8.9 - Radiation doses from German nuclear plants to adults, small children 
and infants in 2006 (ICRP model calculation). 



108 



ECRR Proceedings Lesvos 2009 

The official dose estimates seem questionable - a number of solutions are presented. 
Firstly, there could be a possible incomplete registration and measurement of 
radionuclides emitted by NPP. Official dose calculations use simple propagation 
models:a two dimensional Gauss model might be in error up to factor 10. The ICRP 
model for internal emitters might underestimate doses, especially for alfa and low 
energy beta emitters, eg H-3 (See UK Government CERRIE report (2004) on dose 
uncertainties). Therefore official dose estimates might be low by a factor of between 
ten and a hundred. However, we need to explain a factor of 1000. 

It is an implicit assumption that excess leukaemia risk is proportional to dose, but 
this is only justified if the dose-response relationship is linear. Firstly, residents near 
NPPs are exposed to widely fluctuating dose rates over the year, and not to a 
constant low dose rate. Secondly, the shape of the dose-response curve might be 
curvilinear. 



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Druc.K*ass*rrtsHtfirs (XKW N#cHarw*Uh*im 2) 

Figure 8.10- Concentration ofCarbon-14 C02 in air Bq/m3 in the area of south 
German reactors 



109 



ECRR Proceedings Lesvos 2009 



Teratogenic risk 



^Krebs u. Leukamiej 



vererbbare Defekte" 



Spacef fektG 



-^^Funktionsstorungenj langf ristige 

^ - , t , „ . " ■! Reif unesstoruneen 

^gestorte Zellrei fungi 



Wachstumshemmunfti 



i 



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r "^- ^ 

^Fehlbildungeu 



Rcsorptiionen ^\ 



I ; 

intrauterine 

i Fciiheffekte 

(Geburt) 
i 



i 



2 I 6 8 10 12 14 16 1B t 

I — i — i — i — i — i — i — i — r — i — i — i — i — i — i — \ — i — i — i — i (Tage p.c.) 



Figure 8.11 - Teratogenic risk: Prenatal induction of radiation damage in the 
mouse 



In Fig 1 1 we see the development of different end points as dose increases. Early 
effects in the 0-6 week period of foetal development results in resorption. In the 
organogenesis period of 6 to 12 weeks there can be malformation induction with 
intrauterine deaths. These are the early effects of intrauterine exposure. Late effects, 
including cancer and leukemia result from exposures after 8 weeks but also during 
the 14+ week period. 

The studies' assumptions are as follows: 

1 . annual background dose (excluding radon) -1 mSv/a 

2. additional dose from NPP: -0. 1 mSv per year 
(ie -10-100 times larger than official estimates) 

3. leukaemia 100% radiation induced 



110 



ECRR Proceedings Lesvos 2009 

4. prenatal origin of leukaemia in children under age 5 

5. discontinuous emissions from NPPs 

6. non-linear dose response 

Following the Chernobyl accident, a significant association of perinatal mortality 
with the caesium burden of pregnant women in Germany was found. The dose 
response is curvilinear with a best estimate of 3.5 for the power of dose (95% CI: 
1.5-7.5) [3]. Significant association between stillbirth rates and caesium ground 
deposition in Bavaria. A 3rd degree polynomial yields the best fit to the data 
{Korblein, unpublished). Significant association of stillbirth rates in Cardiff, GB, 
with the tritium emissions of Amersham pharmaceutical plant. A linear- quadratic 
model best describes the dose response relationship {Korblein, unpublished). 



183.0 



180.0 




1.5 2 2.5 3 3.5 4 4.5 5 5.5 
power of dose 



6 5 



Figure 8.12 - Power of dose in West German mortality data 



111 



ECRR Proceedings Lesvos 2009 



4 - 



8 



i - 



power of dose = 4 




M-Wdlll 




tmi* 



Figure 8.13 - Dose-effect relationship 



i 




tiiiK 



Figure 8.14 - Dose-effect relationship 

The discovered excess relative risk (ERR) depends on the power of dose n. For n = 
2.5, 4, and 6, the results for ERR are 0.3, 0.6, 1.2. The KiKK study found ERR=0.6 
for all cancers and ERR=1.2 for leukaemias. 



112 



ECRR Proceedings Lesvos 2009 



35 



Mi 



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& 

I 20 



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VnultovichTTx 






r 


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I 




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^ 


*- 





OjO 0,3 G.ti 0,9 1.2 L5 I.S 2.1 2,4 

Individual clost/Mtsiii d«*r in villa^r 



2,7 30 



FIG. 4.1 1. Frequency distributions of monthly effective externa! doses of individual persons 
as measured in summer 1993 with TL dosimeters in four villages of the Bryansk Obiast 
(points/ and calculated by the stochastic model (curve). Doses are normalized to the 
arithmetic mean of the individual doses determined for each of the villages. From Golikov 
et al. (2Q02y 

Figure 8.15 - Frequency distribution of doses 

From these results, we can attempt to derive a dose-response curve. 
We assume: 

• Random distribution of doses in a cohort: 

lognormal distribution with median dose x=ju and standard deviation o\ 
density function/^ = l/(x*a*(27r) 1/2 )*exp(-(ln(x)-ju) 2 /2(j 2 ) 

• Random distribution of radiation sensitivities: 
cumulative lognormal distribution function g(x) 

• Effect in dose interval (x,x+dx) is ~f(x) *g(x) *dx 



113 



ECRR Proceedings Lesvos 2009 




Figure 8.16 -Distribution curves 




3 4 

dose [mSv] 



Figure 8.17 -Numerical calculation of dose effects 

The sum effect is the integral effect of radiation exposure of a population to median 
dose x is proportional to the area under the red curve. In the following graphs, the 
results for median doses of 1.0, 1.2, 1.4, 1.6, and 1.8 mSv and o=0.3 are plotted 
as a function of dose. 



114 



ECRR Proceedings Lesvos 2009 



13 



0.12 
0.10 
0.08 
0.06 
0.04 
0.02 
0.00 



/ 4tB8i&!*= 



y= D.0C.W* 4.9.^ 00550S> 




00558 



0.2 0.4 0.6 0.S 1 1.2 1.4 1.6 1.S 

I }raKmerijan TmSv] 



Figure 8.18 - Dose response relationship: Box-Tidwell model: y=x A n (dose to the n- 
th power) 



14 



0.12 - 

0.10 - 

_ 0.08 - 

1 , 

^ 0.06 - 
0.04 - 
0.02 - 
0.00 - 




Figure 8.19 - Dose response relationship (Regression model: lognormal distribution 
function) 





estimate 


SE 


z-value 


p-value 


(Intercept) 


-1.0600 


0.1310 


-8.0916 


0.0000 


(11 


-2.1110 


2.7950 


-0.7553 


0.4501 


&2 


13.0610 


8.1320 


1.6061 


0.1082 



115 



ECRR Proceedings Lesvos 2009 




30 40 50 

Abstand vom KKW [km] 



70 80 



Figure 8.20 - Linear-quadratic regression model (RR=exp(fil/r+fi2/r 2 )) 



3 D 




o.oo o.or* o.io o.irs 0.20 0.23 0.30 0.33 0.40 

reciprocal distance = dose proxy 



Figure 8.21 - Linear-quadratic regression model (non linear dose response) 

The mathematical form of the dose-response relationship is a cumulative lognormal 
distribution function. The only assumption for the calculation is that both the doses 
and the radiosensitivities are randomly distributed in a population. The present 
model, together with revised dose estimates, has the potential to explain the size of 
the increased childhood leukaemia observed near German NPPs. 



116 



ECRR Proceedings Lesvos 2009 



References 



l.SpixC, SchmiedelS, KaatschP, Schulze-Rath R, Blettner M, (2008) Case- 
control study on childhood cancer in the vicinity of nuclear power plants in 
Germany 1980-2003. Eur J Cancer 44 , pp. 275-284. 

2. Baker PJ and Hoel DG (2007) Meta analysis of standardised incidence and 
mortality rates of childhood leukemia in proximity to nuclear facilities. Eur. J. 
Cancer Care 16 355-363 

3. Korblein A, Kiichenhoff H in Radiat Environ Biophys 1997 Feb;36(l):3-7. 



117 



ECRR Proceedings Lesvos 2009 



9 

Estimation of Residual Radiation Effects on Survivors of 
the Hiroshima Atomic Bombing, from Incidence of the 
Acute Radiation Disease 



Prof Shoji Sawada 

Nagoya University, Japan 

Abstract : The effects of exposure due to radioactive fallout on the survivors of the 
Hiroshima atomic bomb are estimated by analyzing the incidence rates of acute 
radiation diseases, depilation, purpura and diarrhea, among the survivors. It is 
found that the effects of radiation exposure due to the fallout exceeds, on the 
average, the primary radiation effects in people who were beyond about 1 .2 km 
from the hypocenter of the Hiroshima bomb. The average effects of radiation 
exposure from the fallout increases with distance from the hypocenter, reaches a 
peak at around 1.2 km, and then decreases gradually for farther distances but 
remains even at about 6 km. The peak value of estimated effective exposure from 
fallout are comparable with that of acute external exposure of gamma ray doses 
around lGy. The fact that the effects of residual radiation estimated from the 
incidence rate of acute diseases are significantly larger than physically measured 
residual radiation doses suggests that the main effects resulting from residual 
radiation were caused through internal exposure, especially intake of radioactive 
small particles among fallout by ingestion and inhalation. 



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ECRR Proceedings Lesvos 2009 




i Z 3 



§1 Introduction 

Doses of the primary radiation emitted within one minute after from the atomic 
bombs exploded on Hiroshima and Nagasaki cities are well estimated by the 
Dosimetry System 2002(DS02) 1} in the regions within 1.2 km from the hypocenter, 
estimates which are supported by experimental measurements on irradiated 
materials. On the other hand the residual radiations which were emitted one minute 
later or more from the bomb explosion have been not clarified well compared to the 
primary radiation. There are two origins of the residual radiations. One is from the 
fallout and the other from neutron induced radioactive substances. Estimates of 
fallout radiation dose that have been made so far are based on measurements of 
radiation emitted from radioactive matter resulting from radioactive fallout in rain 
which had been absorbed into soil and retained. However, these measurements had 
been carried out after a big fire involving the whole of Hiroshima city and also 
following major typhoon events . It follows that these measurement detected only a 



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ECRR Proceedings Lesvos 2009 

small fraction of the radioactive matter which remained without having been washed 
away. Furthermore, unlike the nuclear atmospheric tests, in Hiroshima and 
Nagasaki radioactive fine particles existed in the fallout, filled the air, were not 
measured and were carried away by the wind. In addition, effects of residual 
radiation resulted from both external and internal exposure through intake of 
radioactive microscopic particles by inhalation and ingestion. In general, physical 
measurements of these exposure effects were not done and quantification through 
measurement is now difficult. These facts imply that there are severe limitations for 
the estimation of the residual radiation doses delivered by the Hiroshima atomic 
bomb by physical methods. 

There have been many investigations related to acute radiation diseases 
among atomic bomb survivors, both from immediately after the bombing and later 
on, and all results of these investigations show that acute diseases such as depilation, 
purpura and diarrhea, etc. appeared even in regions 2 km or more distant from the 
hypocenter. The fact that the diseases occurred among survivors who were present 
in the regions where the primary radiations scarcely reached suggests that they 
should be explained in terms of fallout radiation. In order to grasp residual radiation 
effects comprehensively it is possible to investigate the results of such examinations 
of acute diseases as well as risks of chronic diseases, frequency of chromosomal 
aberration, i.e. biological effects caused by radiation exposure among survivors. 

If initially the relation between exposed doses and incidence rates of a specific 
acute disease condition can be determined then it is possible to obtain the effective 
dose of exposed radiation necessary to cause that condition. Then by subtracting the 
primary prompt radiation dose from this resulting effective dose we will obtain the 
mean effective dose for the condition of interest due to exposure from fallout 
radiation alone. This biological dosimetry method will be useful to examine 
combined effects from both residual external and internal exposure to the survivors. 

In this paper, in order to clarify the effects of residual radiation from fallout, 
the incidence rates of acute radiation diseases among survivors of the Hiroshima 
atomic bomb are analyzed. The fact that the calculated effects of residual 
radiation estimated from the incidence rate of acute diseases are significantly larger 
than physically measured residual radiation doses suggests that the main effects 
resulting from residual radiation were caused through internal exposure, especially 
the intake of radioactive small particles among fallout by ingestion and inhalation as 
well as external exposure from radioactive particles clinging on skin or clothes. 
The results of the effects of residual radiation obtained here from the incidence rates 



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ECRR Proceedings Lesvos 2009 

are consistent with studies of frequency of chromosomal aberration and mortality 
and incidence rates of chronic diseases. 

§2 Relation between Incidence Rate of Depilation and Exposed Dose 

In this section a relation will be derived between the exposure dose and the 
incidence rates of depilation, a typical acute radiation disease. Stram and Mizuno 2) 
first derived a relation between the exposure dose of the atomic bomb primary 
radiation and the incidence rates of depilation. They employed the results of the 
Life- Span- Study (LSS) group of the Atomic Bomb Casualty Commission (ABCC, 
the predecessor of Radiation Effect Research Foundation, RERF) obtained around 
1950 for the heavy depilation (above 67 %) which appeared within 60 days after the 
detonation of the bomb. In Fig. 1 their results are shown by small black circles 
where the horizontal axis is scaled by the primary radiation dose estimated by the 
Dosimetry System 1986 (DS86) 3) . As shown in Fig. 1 the incidence rate increases 
slowly up to 0.85 Gy of the primary radiation dose, then rapidly increases above 1 
Gy and exceeds 50 % at around 2.4 Gy. However, beyond 3 Gy the rates do not 
increase and even decrease as dose approaches 6 Gy. This unnatural behavior of the 
incidence rates in the high dose region can be explained by the fact that the LSS 
group contains only survivors who could survived though they had exposed near or 
more of a half-death-dose about 4 Gy as pointed up by Stewart et. al. 4) 



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ECRR Proceedings Lesvos 2009 



^ 

o^ 



CD 

+-> 

C 


O 



Relation between Incident Rate of Depilation and 
Exposed Dose 




• Inc dent Rate of LSS by SM 
-Modified D istrbutbn of LSS 
Fitby NormalD istrbutbn 

o T ransplant Experm ent by KSTS 
F it by N orm a I D istrbutbn 



2 3 4 

Exposed Dose Gy 



Fig. 9.1 Relation between incidence rates of depilation and exposure dose. Closed 
circles are incidence rates of depilation among LSS-Hiroshima group against 
primary exposure dose obtained by Stram and Mizuno. Full line is the fitted curve 
of the modified normal distribution to the closed circles below 3 Gy region. Open 
red circles are incidence rates from the transplant experiment by Kyoizumi et al. 
The red full line is the normal distribution fitted curve. 

Incidence rates of depilation shown by open circles in Fig. 1 are those obtained by 
Kyoizumi et al. 5) by means of radiation exposure to transplantated human head skin 
onto mice. As seen in Fig. 1 the incidence rates increase very slowly in the low 
exposure region compared to those given by Stram and Mizuno and increase to 95.5 
% and 97 %, almost 100 % at exposure of 4.5 Gy. From experimental studies with 
animals it is known that most of dose dependence of incidence rates or death rates 
are represented by a Normal (Gaussian) distribution. The incidence rates given by 
Kyoizumi et. al. over the whole range of the exposure region can be fitted well by 
the Normal Distribution with an expectation value of 2.751 Gy and Standard 
Deviation 0.794 Gy, i.e. N(2.751 Gy, 0.794 Gy), and shown by a solid curve in Fig. 
1. The Normal Distribution N(2.751 Gy, 0.794 Gy) will be referred to as the KSTS 



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ECRR Proceedings Lesvos 2009 

relation and adopted as the relation between incidence rates of depilation and 
exposed dose in the following analysis. 

The incidence rates of depilation below the 3 Gy exposure region given by Stram 
and Mizuno can be fitted by a Normal Distribution N(2,404 Gy, 1,026 Gy) except 
for the region near zero dose. This Normal Distribution, however, can not reproduce 
the increase of the incidence rates in the region near zero dose represented by black 
circles which are rapid in comparison with the KSTS relation. The broken line 
shown in Fig. 1 is generated by the modified normal distribution which is obtained 
by multiplying another normal distribution function N(0.165 Gy, 0.1155 Gy) to the 
original normal distribution function N(2,404 Gy, 1,026 Gy). This different 
behavior of the incidence rates found by Stram and Mizuno from that of Kyoizumi 
will be explained later by taking account of fallout exposure. 

In the following the incidence rates of acute diseases of the region below 1 km 
from the Hiroshima hypocenter are excluded from analysis because most of people 
bombed within 1 km were killed and the reported rates are statistically unreliable. 
Furthermore, the total sums of gamma ray and neutron dose at 1 km are 4.48 Gy 
from the estimation by DS02, by which the calculated incidence rate attained almost 
100 % on the basis of the assumed normal distribution of the KSTS relation. 

§3 Estimation of Fallout Exposure from Incidence Rate of Depilation among 
LSS Group 

In this section the radiation exposure effects from the fallout of the Hiroshima 
bombing are estimated on the basis of incidence rates of depilation among the LSS- 
Hiroshima group. Preston et al., 6) reported separately the incidence rates of 
depilation of Hiroshima and Nagasaki survivors among the LSS group. In Fig. 2. 
the dependence of the incidence rates of depilation of 58,500 Hiroshima survivors 
among the LSS on distance from the hypocenter is shown by squares. The incidence 
rate of 100% at 0.75 km is scaled out of the frame. The black circles and a dashed 
line in Fig. 2 for the primary radiation dose dependence are translated into distance 
dependence by use of the DS86 estimation neglecting shielding effects and are 
plotted by black diamonds and a broken line. If the shielding effects are taken into 
account the diamonds shown in Fig. 1 will move to left toward hypocenter and the 
difference between the squares will increase. In the following it is assumed that the 
systematic difference between squares and diamonds shown in Fig. 2 represents 
exposed effects from fallout radiation. 



123 



ECRR Proceedings Lesvos 2009 

In the analysis of the incidence rate of depilation it is assumed that the total 
exposed dose D(r) at distance r km from hypocenter is given by a sum of the 
primary radiation exposure cP{r) with shielding effects represented by a parameter c 
and exposure F(r) from fallout radiation as 

D(r) = cP(r)+F(r). (1) 

The formula for exposure from fallout radiation F(r) is assumed as 

F(r) = ar exp(V lb 2 ) + d (2) 

where parameters a, b, and d represent magnitude, extension and distance 
independent component of fallout exposure effects, respectively. Theoretical 
incidence rates are calculated from the exposure dose D{r) given in (1) by use of the 
KSTS relation between incidence rate and exposed dose. A set of four parameters in 
(1) and (2) is determined so that the% 2 value takes minimum which represents fitness 
of the calculated incidence rates to those of LSS group and obtained as c = 0.522, a 
= 0.808 Gy/km, b = 2.062 km, and d = 0.786 Gy. The resulting fitted incidence 
rates are shown by a bold line in Fig. 2. 



124 



ECRR Proceedings Lesvos 2009 



80 



70 



60 



50 



40 



30 



20 



10 



Fig. 


2 

i 


Incident Rates of Epilation (Hirosh 


—■ :— Irr 


i i i i i i i i i i 


i 1 

. 1 1 

1 

• 

4 


1 

r- 

M 

L|_- 

i 
t 


♦ St ram-Mi zuno (Pr imary Rad. ) 

Fit to Stram-M i zuno (Pr imary Rad) 1 

□ ABCC-RERF-LSS (H i rosh i ma) 

p; + + ARpp DCRF 1 ^ fH i rnch i ma") ' 




i i l lu nuuu i\i_i\i LOO vi i i r Ubl i i nidy , 








!'!!!!! 


♦lli 

. i Ll • L ' L ' L ' L ' ' 




"-♦ 




■ — ■ 
_ — . 

■ — ■ 
_ — . 

■ — ■ 


. 1 L _iT 1 L 1 L 1 L 1 L 1 1 

: i\ : : i i i i 

i L - U J L • L • L • L • ' 


: i \: : : : : : 


" 1 r ~~i~\ r ' r ' r ' r ' ' 

i \: b i i i i i 

. 1 i. — 4^.1 — -V^j- - — i i- 1 i- 1 i- 1 i 

t "--t*. 4~^ — D-H_l THr-n — D— r 



12 3 4 
Distance from Hypocenter km 



Fig9.2. Incidence Rates of Depilation of LSS Hiroshima. Squares indicate the 
incidence rates of depilation among Hiroshima survivors of the LSS. Full line 
shows the curve fitted by formula (1) and (2) with the minimum value of/ 2 of about 
10 which is below 14.1, the lower limit of 5% of rejection area ofx distribution of 
freedom degree (FD) 7. Black diamonds shows the approximate incidence rates 
corresponding to the primary radiation. 



125 



ECRR Proceedings Lesvos 2009 

The doses of total, primary and fallout exposure, D{r), cP{r) and F(r), with the 
obtained parameter set are shown by a bold dashed curve, a thin dashed curve and a 
bold solid curve, respectively and the primary doses estimated by DS02 are also 
shown by a thin solid line in Fig. 3. As seen in Fig. 3, the effects of fallout exposure 
increases with distance from hypocenter up to 1 km, but this has large ambiguity 
because the incidence rates in the region below 1 km were not employed in the 
present analysis. Exposure from the primary radiation rapidly decreased with 
distance from the hypocenter and at about 1.2 km the fallout effects cross over that 
of primary radiation. The estimated exposure from fallout radiation reaches about 
1.5 Gy at around 1.45 km then decreases slowly. Beyond 4 km the exposure effect 
of fallout takes an almost constant value of 0.79 Gy. This result from the incidence 
rates of depilationm, one of the actual accepted and universally agreed conditions of 
the bombed survivors, indicates overwhelming effects of fallout beyond about 1.5 
km from the hypocenter of Hiroshima. For example at 2.25 km and 2.75 km from 
hypocenter the dose estimation of the primary radiation by DS02 are 0.0302 Gy and 
0.0053 Gy while the incidence rates of depilation among the LSS-Hiroshima at these 
distances are 3.5 % and 2.1 %. The estimated fallout exposure effects from these 
incidence rates is 1.34 Gy and 1.16 Gy, about 44 and 219 times of the DS02 primary 
radiation. 

The maximum cumulative exposure from fallout of the Hiroshima bomb has been 
considered hitherto between 0.006 and 0.02 Gy in the Koi-Takasu region mentioned 
in the DS86 report and which are shown by cross marks in Fig.3. These absorbed 
doses were obtained from measurement of radiation from fallout matter retained in 
the soil of these regions which are located between 2 and 4 km to the west of the 
hypocenter where light radioactive fallout rain fell but heavy rain caused by the big 
whole city fire did not. As seen in Fig.3 exposure from fallout estimated from 
depilation incidence rates in 2 to 4 km region are 1.4 Gy to 0.85 Gy which are 40 to 
230 times of physically obtained values. This large discrepancy suggests that the 
physically measured values are only measurements of a part of fallout and that large 
effects of internal exposure should be taken into account which can be deduced only 
by the biological methods. 



126 



ECRR Proceedings Lesvos 2009 



2.5 



1.5 



0.5 





Fig 


■ 3 ft 


lout Exposure 


from 


Incid 


ent Rates of Ep i 


at 


ion 














1 


i i i i i i i i i i i i i i i i i i i i 




... 


... 


I 

1 


i i i 
i i i 


i i i i i i i i i i i i i i i i i i i i 


. i _ _ i 

■ T 1 

■ + 1 

■ T " _ I 


L _ _ 1 1 

1 l 1 

1 l 1 

r — i 1 

l: : : 


"" O^— Fallout Exposure (Kyoizumi etal) 

• Primary Exposure (Kyoizumi eyal) 

— O^ Total Exposure (Kvoizumi etal) 








'l 


li ■ 1 

i L ! 




ary Radiation Dose by DS02 
Physical Measurement of Fallout 


... 


... 




• 1 

-- + I- 
! i 

- - T - - 

• 1 


1 : 

4_ _ « • 


P \ i in 

N/ M i-i u 


A Max. 














-jl- 

_ _ j. 4_ 


i\ : : : 




























! i 


IE: 




























; i 


:.\.J..J.. 




























- - T -|- 


r~-\--i 1 

l__L\_:__j_-j 






















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1 


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! 1 


A: 






















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1 


i_l_jl__L__!__J_T^ 










































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r 






















i! \ ! ! ! 




























! il 1 ! 












































**< 


>^r- 


=6" 








! } \! 


















■-T--(-Ar- 
__i__Ll__\._J ! 




























i i. 1 i\ 




























. . t A . 




























i \ : : 




























! ! 1% \! ! 




























._{._L-L-VVh-- + 






























£4— 


=^_x- 


i i i 
1 • ' 






i 
, i 





2 3 4 

Distance from Hypocenter km 



Fig.9. 3 Exposure doses (Gy) estimated from the incidence rates ofdepilation among 
the LSS Hiroshima group. Total, primary and fallout exposures are given by bold 
dashed, bold full and thin dashed lines, respectively. The primary radiation 
absorption dose is estimated by DS02 and is shown by thin full line. Physically 
measured maximum exposures from fallout at Koi-Takasu region are shown by 
cross marks. 

The values obtained here are average exposures in the same distant regions from the 
hypocenter irrespective to directions. It is supposed that the fallout fine particles 



127 



ECRR Proceedings Lesvos 2009 

were moved toward northwest direction by wind. To clarify these effects it is 
necessary to carry out a direction dependent analysis. 

§ 5 Estimation of Fallout Exposure from Incidence Rates of Depilation Other 
Examinations than LSS 

In Fig. 4 incidence rates of depilation examined by the Joint Commission for the 
Investigation of the Atomic Bomb 7) and Tokyo Imperial University 8) in 1945 and 
investigated by 0-ho 9) in 1957 are shown together with those of LSS-Hiroshima. In 
investigation by O-ho, all survivors were classified into four types according to 
whether they were exposed indoors or outdoors and did or did not enter within 3 
months into the central region within 1 km from the Hiroshima hypocenter. The O- 
ho examination of the No Entrance case is very important because the exposures 
from the induced radioactive matter in the central region were not included. 

Except for two incidence rates at 2 km and 4 km* 1 by O-ho all the examined 
incidence rates of depilation among the Hiroshima survivors almost coincide with 
each other indicating the reliability of all these investigations. That the rates of the 
LSS-Hiroshima between 1.75 km and 2.75 km are slightly lower systematically than 
the others may be explained by the fact that in the LSS examination depilation is 
defined as only heavy depilation with 67% loss of hair within 60 days from atomic 
bombing. 



** These data at 2 km and 4 km given by O-ho are omitted in the x 2 fitting. 



128 



ECRR Proceedings Lesvos 2009 



80 



70 - 



60 



50 - 



40 - 



30 - 



20 - 



10 



Incident Rates of Epilation (Hiros 




12 3 4 

Distance from Hypocenter km 



Fig.9. 4 Incidence Rates of Depilation among Hiroshima Survivors. The marks □, 
•, x and ▲ are incidence rates examined by ABCC, the Joint Commission, the 
Tokyo Imperial University and O-ho, respectively. The % values fitted to Joint Com. 
and Tokyo Imp. Univ. examinations are 4.2 and 5.6, respectively, compared to 6.6, 
the lower limit value ofl% risk region ofx 2 distribution ofDF I and fitted to O-ho 
case is 3.3 compared to 9.2, the lower limit of 1% risk region of ofx 2 distribution of 
DF2. 



129 



ECRR Proceedings Lesvos 2009 

The same fitting method used in the LSS group is applied for these incidence rates 
of depilation. The resulting sets of parameters from application of formulae (1) and 
(2) are given in Table I. The fitted incidence rates curves are shown by thin dashed 
lines in Fig. 4. The calculated doses of total, primary and fallout exposure, D{r), 
cP(r) and F(r), obtained by fitting to the reported incidence rate curves of depilation 
are shown by a bold dashed curve, a thin dashed curve and a bold solid curve, 
respectively in Fig. 5. 

Table 9. 1 Parameters in formulae (1) and (2) of exposed doses from incidence 
rates of depilation examined ABCC, Joint Commission, Tokyo Imperial 
University and O-ho. 





primary rad. 

exposure 

cP{r) 


fallout radiation exposure F(f) 


c 

shielding 
effect 


a (Gy/km) 
magnitude 


6 (km) 
extension 


d{Gy) 

constant 
part 


ABCC LSS-Hiroshima 
(heavy depilation) 


0.522 


0.808 


2.06 


0.786 


Joint Commission 

(outdoors or Japanese 
house) 


0.600 


1.272 


2.34 


0.300 


Tokyo Imperial 
University 

(outdoors and indoors) 


0.390 


1.330 


2.11 


0.501 


O-ho (indoors, no 
entrance into central 
region) 


0.226 


1.166 


2.06 


0.751 



130 



3 


Fig. 5 
, r i _■ ■ 


Est imat ion 

1 Ul 


Df [ 


Exposure from Incidence Rates of Epilal 






-i-l-ii 

IS 


I 


i i i i i i i i i i i i i i i i 








1 


i i i i i i i i i i i i i i i i 








i 




Fal lout Exposure (LSS-Hi rosh ima) 
• Primary Exposure (LSS-Hi rosh ima) 






i 








i i j j 


j 






ion Dose by DS02 
(Tokyo Emp. Uni v. ) 




2.5 


__: : :_i j 


i i 


Pr i mar y Rad i a I 
^~ ^^~ Total Exposure 


— ! 




: : ii 

' « i_ . _ 






* Primary txposure (J okyo tmp. Univ.; 

A Fal lout Exposure (Tokyo Emp. Univ.) 
^HZr^~ Total Exposure (0-ho) 

° Primary Exposure (0-ho) 

^HZr^™ Fal lout Exposure (0-ho) 
^~ ^^~ Total Exposure (Jo i nt Com.) 

— — • Primary Exposure (Jo i nt Com.) 

^^^^^ Fal lout Exposure (Joint Com.) 






ii . 1 I ' TL . . 

J. 1 1' a 








: : ; i ' 
..J.-.L.J.j.LL 


• : i- : 






2 


: ,ii 

\ \ \ | III 
.. t 

l> 


:V 


- - i 

— i 


— i 














"^h 




::::::: 












P JtTi/i 

- -^/ : i?-/-tl 

t x JJJ_£ J } i 


r \^W \ 


!!!!!!! 










1.5 


^^"\^^ \ 












ll ;__j 






L \l 1 1 1 1 1 1 


j 


1 1--L--I 1 l_ 




i 




















Jl.J— !— 














1 


M ; 

if \ • ' 














// / !/ ! * 


5 

l-U-A-l- 


_ " T " " 


■ - - i r - ^t - ~i~^C^A_ lw^ 




- -T"~T~~r~~i 1 r 










\4\i i 












/ ' / ' 
















\ 
















0. 5 L 


\w \ 


._:_. 


IN 






-- 




7.L. _:._.:... 


\ 










""KY\:" 














■-■;v\i\\Ai-- j 














n 


. _ _ ' ' ' 




_ _ i _ _ 


, — i 

j — i 

1 — i 

1 — 


> 1 


__I__i__L__' ' '_ 

i A 6 A i A L_ 


— 1 


l ! 



2 3 4 

Distance from Hypocenter km 



Fig. 9.5 Estimation of exposures from incidence rates ofdepilation among the 
Hiroshima survivors. Total, primary and fallout exposures are shown by bold 
dashed lines, thin dashed lines and bold full lines, respectively. Marks o, U, □ and 
□ indicate examined by ABCC, Joint Commission, Tokyo Imperial University and O- 
ho. 



131 



ECRR Proceedings Lesvos 2009 

The peak values of exposure by fallout are found to lie between 1.58 Gy and 1.78 
Gy slightly higher than that of the LSS as expected from the small difference among 
incidence rates. In the region beyond 3 km from the hypocenter the fallout exposure 
estimation from O-ho's incidence rates is almost similar to those from the LSS. A 
rapid decrease of fallout exposure dose is seen beyond 3 km in the case of the 
examination by the Joint Commission, where incidence rates of depilation in the 
region 4 ■ 5 km and beyond 5 km are zero based on very few survivor examination 
compared with LSS. 

§6 Comparison of Fallout Exposure Estimated from Incidence Rates of Three 
Different Acute Diseases 

In the following it will be examined whether the incidence rates of three different 
acute diseases, depilation, purpura and diarrhea can be explained by the same 
exposure dose or not. The incidence rates of depilation, purpura and diarrhea among 
Hiroshima survivors who were exposed indoors and did not enter the central region 
examined by 0-ho 9) are shown in Fig. 6. As is seen in Fig. 6 incidence rates of 
purpura shown by closed circles are of similar behavior to those of depilation shown 
by squares. Then for the incidence rate-exposure relation of purpura the same 
normal distribution of depilation is used. Incidence rates of diarrhea shown by 
triangles are very large compared to depilation or purpura in the distant regions 
beyond 1.5 km where the fallout exposure gave significant effects. The incidence 
rates of diarrhea were rather small in the short distance regions where the primary 
radiation exposure dominated. Therefore in the case of diarrhea, a larger 
expectation value for the normal distribution than those of depilation and purpura is 
required for external exposure from the primary radiation and smaller expectation 
value is required for the fallout exposure. The adapted expectation values and 
standard deviations are listed in Table II and were obtained by multiplying the ratios 
shown there. By use of the normal distributions with expectation values and 
standard deviation given in Table II the incidence rates of depilation, purpura and 
diarrhea in Fig. 6 are fitted and the resulting incidence rates are displayed by thin 
dashed, solid and chain curves for depilation, purpura and diarrhea, respectively 
whose parameters of formulae (1) and (2) are listed in Table III. 



132 



ECRR Proceedings Lesvos 2009 



Table 9. II Normal distributions of incidence rate-exposure dose relations of 
acute radiation diseases 



acute disease 


ratio 


expectation 
value 

(Gy) 


standard 
deviation 

(Gy) 


depilation 


1 


2.751 


0.794 


purpura 


1 


2.751 


0.794 


diarrhea 


primary radiation 


1.1 


3.026 


0.873 


fallout exposure 


0.72 


1.981 


0.572 



Table 9.III Parameters in formulae (1) and (2) of exposed doses from incidence 
rates of depilation, purpura and diarrhea 





primary rad. 

exposure 

cP(r) 

c 

shielding 
effect 


fallout radiation exposure F(r) 


a (Gy/km) 
magnitude 


b (km) 
extension 


d(Qy) 

constant part 


Depilation( 1,0.52) 


0.5 (fix) 


0.984 


2.07 


0.855 


Purpura (3, 3.2) 


0.5 (fix) 


0.995 


2.36 


0.713 


Diarrhea (5,12.7) 


0.511 


0.959 


2.37 


0.743 



133 



Fig. 6 Incidence Rates of Acute Diseases (0-h 



80 



70 



60 



50 



40 



30 



20 



10 



□ Dep i I at i on (0-ho) 
— ■ — Fit to Inc. Dep i I at ion 

O Purpra (0-ho) 

Fit to Inc. Purpra 

A Diarrhea (0-ho) 
— -*---Fit to Inc. Diarrhea 




12 3 4 
Distance from Hypocenter km 



Fig. 9.6 Incidence rates of acute diseases among survivors who were exposed 
indoors and did not enter into the central region within 1 km from the hypocenter 
within 3 months. Marks □, o and □ indicate incidence rates of ^epilation, purpura 
and diarrhea, respectively. Full line, dashed line and chain line are fitted curves to 
the incidence rates of ^epilation, purpura and diarrhea with % values 0.52, 3.2 and 
13.3 compared to 9.5, 12.6 and 16.9, the lower limit of 5% rejection area of/ 2 
distribution ofFD of 4, 6 and 9, respectively. 



134 



ECRR Proceedings Lesvos 2009 

In this analysis of depilation and purpura the shielding effect parameter c is fixed to 
0.5 and the data of incidence rates of these diseases at 1 km are omitted because if 
these data of depilation and purpura are used, unnaturally small values of c, 0.22 and 
0.23 are obtained. These unnatural small values at 1 km may be explained by a 
similar reason appeared in the incidence rates of depilation among the LSS in the 
large exposed region given by Stram and Mizuno i.e. many died. 

The results of exposure doses calculated from the calculated parameters listed in 
Table III are shown in Fig. 7. As seen in Fig. 7 incidence rates of three entirely 
different acute diseases are reproduced with high accuracy by almost similar 
exposure doses. This fact tell us that depilation and diarrhea as well as purpura 
occurred in the regions where the primary radiation could scarcely reach and were 
caused by fallout radiation not by mental shock nor by poor sanitary conditions. 

The fact that the expectation value of the normal distribution of diarrhea incidence 
is small for fallout exposure while large for the primary exposure can be explained 
by means of difference between external and internal exposures as follows. In the 
case of fallout exposure radioactive fine particles and radionuclides with specific 
affinity for biological materials and tissues among fallout were taken into body, 
reached directly to intestinal wall and were retained there for a period of time. Then 
the emitted radiation of weak penetration power gave dense ionizations and caused 
heavy damages in the thin membrane and diarrhea followed. The exposure was 
chronic as the particulate and chemical radioisotopic material (e.g. Sr-90, Cs-137) 
was retained for some time. On the other hand in the instantaneous acute primary 
radiation exposure case only strong penetrative radiation such as gamma ray could 
reach from outside of body to intestinal wall but passed away through thin 
membrane leaving scarcely any damage. 



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ECRR Proceedings Lesvos 2009 



Fig. 7 Exposed Doses from Acute Diseases (0-ho) 



Primary Radiation (DS02) 
Total Exposure (Depilation) 
Primary Exposure (Depilation 
Fa I I out Exposure (Dep i I at i on) 
Total Exposure (Purpra) 
Primary Exposure (Purpra) 
Fallout Exposure (Purpra) 
Total Exposure (Diarrhea) 
Primary Exposure (Diarrhea) 
Fallout Exposure (Diarrhea) 




1 



Distance from Hypocenter km 



Fig. 9.7 Exposed doses from acute diseases. Attached marks o, ■ and □ indicate 
estimations from incidence rates of depilation, purpura and diarrhea. Total, 
primary and fallout exposure are specified by bold dashed, thin dashed and bold full 
lines, respectively. The primary radiation dose given by DS02 is represented by thin 
full line. 



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ECRR Proceedings Lesvos 2009 

§7 Summary and Discussion 

As described in the foregoing sections the exposure effects of fallout of 
Hiroshima atomic bombing estimated from incidence rates of acute diseases among 
survivors are very large and extended to a wide area. Exposure effects of fallout 
radiation were greater than the effects of primary prompt radiation beyond about 1.2 
km from the hypocenter and decreased slowly with distance remaining about 
0.7-0.8 Gy even at 6 km. The maximum exposure effects from fallout 0.02 Gy at 
Takasu, the special region located at 3 km west from the Hiroshima hypocenter were 
obtained from physical measurement of radiation emitted from radioactive nuclei 
brought by fallout rain and retained in the soil. Fallout exposure effects estimated 
from acute diseases lie between 1.1 Gy and 1.3 Gy at 3 km distant from the 
hypocenter irrespective of direction from the hypocenter. This large difference 
between physical measurement and biological estimations of fallout exposure imply 
that the main exposure effects were either caused by fallout fine particles widely 
distributed resulting in internal exposure due to their intake or to a error in the 
currently accepted radiobiological effectiveness of certain ingested or inhaled 
isotopic components of the fallout. 

Since the various examinations of incidence rates of acute radiation induced 
diseases analyzed here give almost the same results on fallout exposure then the 
greatest ambiguity of exposure doses obtained will arise out of an ambiguity of the 
relations between the incidence rates and exposure dose used here, that is, 
ambiguity of the expectation values and values of the standard deviation of the 
generated normal distributions. However, if the fallout radiation exposure of 1.0 to 
1.5 Gy obtained here is added to the primary prompt radiation exposures in the 
region between 1 Gy and 3 Gy corresponding to exposure distances between 1.0 km 
and 1.2 km and added to incidence rates of depilation of about 10 %, which 
corresponds to the difference between the solid line and the broken line in the region 
between 1km and 1.2 km in Fig. 2, then the broken line in Fig. 1 shifts to the higher 
dose direction and higher incidence rate direction and almost overlaps with the full 
line obtained by Kyoizumi et al. The unnaturally rapid increase of incidence rate of 
depilation in near zero dose region of the Stram-Mizuno relation shown in Fig. 1 can 
be correlated to the decreases of incidence rates in the region between 1.5 km and 3 
km distant from the hypocenter where the primary radiation exposures were between 
to 1 Gy. This fact supports the conclusion that the relation between the incidence 



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ECRR Proceedings Lesvos 2009 

rates and exposure dose among survivors is not much different from those used here 
on the basis of the relation given by Kyoizumi et al. 

The results obtained here do not contradict results of investigations of 
chromosomal aberration among survivors. The frequency of chromosome 
aberrations in circulating lymphocytes of survivors of the Hiroshima bombing was 
compared with 11 non-irradiated healthy controls visiting the Japan Red Cross 
Central Hospital in Tokyo between April 1967 and March 1968 by Miyata and 
Sasaki 10) . It was found that more than 1.6 km from the hypocenter, the effects of 
exposure from fallout estimated from frequency of chromosomal aberration 
exceeded that of primary irradiation. If we note that the estimated dose based on the 
frequency of chromosomal aberrations in circulating lymphocytes represents the 
effects averaged over the whole body and that local effects from insoluble 
radioactive particles or other internal isotopic exposures which are considered in the 
incidence rates of acute diseases, are not included, then the present results from 
acute diseases do not contradict to that obtained from chromosomal aberration. 

Present results from incidence rates of acute diseases also do not contradict to the 
similar results of investigation obtained from chronic after effects in the LSS of 
RERF. Schmitz-Feuerhake n) had obtained the standard relative risks, mortality 
ratios, and incidence rates of various diseases in the LSS control groups, who were 
exposed to less than 0.09 Gy according to the 1965 tentative dosimetry 
system(T65D), compared with all Japanese. The standard risks for mortality from all 
causes and all diseases are less than unity (this was in the early 1980's results of 
survivors but are now almost unity or slightly larger than unity) indicating that 
control cohort of LSS were healthier than the Japanese average. However, the high 
relative risk of death from leukemia and cancer of the respiratory system and the 
incidence of thyroid and female breast cancer in the control group show that they 
had been affected by fallout radiation. Recent study by Watanabe et al. 12) on the 
mortality of the LSS Hiroshima group from all diseases and various cancers 
compared with those of all inhabitants of Hiroshima prefecture and with those of all 
Okayama prefecture, a neighbor prefecture of Hiroshima, indicates comparable 
effects of fallout exposure with the present estimation among extremely low 
exposure groups (exposed from primary radiation less than 0.005 Sv) and low 
exposure groups (exposed from primary radiation between 0.005 Sv and 0.1 Sv) of 
the LSS. 

By the use of the same method employed here similar effects from the residual 
radiation exposure can be estimated for the survivors of Nagasaki as well as for the 



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ECRR Proceedings Lesvos 2009 

'entrant survivors' who were entered into regions about 1 km from the hypocenter 
after the explosion of atomic bomb and who were exposed to residual radiation 
emitted by induced radioactive matter. The estimated results from these cases will 
be reported elsewhere. 
References: 

1) R. W. Young and G. D. Kerr, Reassessment of Atomic Bomb Radiation 
Dosimetry for Hiroshima and Nagasaki — Dosimetry System 2002, Vols. 1 and 2, 
RERF, 2005. 

2) D. O. Stram D. O. & Mizuno S. Radiation Research 117, 93-1 13 (1989). 

3) W.C. Roesch, US-Japan Reassessment of Atomic Bomb Radiation Dosimetry in 
Hiroshima and Nagasaki: Final Report, Vol. 1, RERF, 1987. 

4) A.M. Stewart and Keneale G.W., Health Phys. 58, 782-735 (1990): 64, 467-472 
(1993); Int J Epidemiology, 29, 708-714 (2000). 

5) S. KyoizumiDT. Suzuki, S. Teraoka and T. Seyama, Radat Res 194, 11-18 
(1998). 

6) D. L. Preston Mabuchi K., Kodama K., Fujita S., Magazine of Nagasaki Medical 
Society (in Japanese), 73, 251-253 (1998). 

7) A. W. Oughterson et al, "Medical Effects of Atomic Bombs— The Report of the 
Joint Commission for the Investigation of the Atomic Bomb in Japan" U.S. AEC, 
1951D 

8) The Science Council of Japan "Collected Reports of Investigation of Atomic 
Bomb Disaster Vols. 1 and 2" (in Japanese), Japan Science Promotion 
Association, 1953. 

9) G. O-ho; "Iji-shinpo" (in Japanese) No. 1746, 21-25,(1957). 

10) M. S. Sasaki, H. Miyata; Biological dosimetry in atomic bomb survivors. Nature 
1968;220:1189-93. 

11) I. Schmitz-Feuerhake, I., Health Phys. 44, 693-695 (1983); Schmitz-Feuerhake, 
I., & Carbonell, P., Publication SM-266-23. ViennaTAEA, 45-53 (1983). 

12) T. Watanabe, M. Miyao, R. Honda and Y. Yamada; Environ Health Prev Med., 
Vol. 13,No.5(2008). 

Editor's note: 

Prof Sawada also spoke at the conference about Nagasaki and gave some slides. 
These are reproduced below: 



139 



ECRR Proceedings Lesvos 2009 



Nagasaki effects 




Figure 9.8 - Measurement ofPu239 in soil brought by fallout rain of Nagasaki 
bomb (Bq/hg soil) 

In Nagasaki, as opposed to in the contamination after Hiroshima, the fire rain was 
much less powerful. As a result, the radioactive fallout matter did not wash out 



140 



ECRR Proceedings Lesvos 2009 



Incidence Rates of Acute Diseases by Nagasaki 
Bombing 



45 
40 
35 
30 
25 
20 
15 
10 













o epilation 
□ purpra 




.- -. m m J. 






~ .. » .. L m. m . 


— ■ — purpura tit 

A diarrhea 
— * — diarrhea fit 


1 .. _. _. J 
















m - ~ " T ~ "* " 1 

.. m. - .. * _ - ..4-.--- 




*il 








____J.-.A__ 




"■fff" 




















1 ■ ■ ■ m ■ "B 






"^1*1 


— : — : — r^h — ci : 

, . i 



5 10 

distance from hypooenter (km) 



Figure 9.9 - Estimation of Exposure due to the Fallout of Nagasaki Bomb in terms 
of Incident Rate of Acute Radiation Disease 

Combined Analysis of Examination of Acute Diseases for Nagasaki City (<4.5 km) 
by Nagasaki Medical College 194. For Enlargement of Designated Region ofA- 
Bombing. Peripheral of Nagasaki City (Av. 9.5 km) by Government of Nagasaki 
City. Surroundings of Nagasaki City (Av. 11.3 km) Local Gov. Town & Village) 

In Figure 9, the closed circles, squares and triangles show incident rates of epilation, 
purpura and diarrhea, respectively as the acute diseases among survivors of 
Nagasaki city (< 4.5 km from the hypocenter) examined in 1945 by the Nagasaki 
Medical College and those incident rates examined by the local government of 



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ECRR Proceedings Lesvos 2009 

Nagasaki City ( average distance is 9.5 km from the hypocenter) and surrounding 
towns and villages of Nagasaki (average distance is 11.2 km from the hypocenter) 
which were published in 2000. 



Exposure by Nagasaki Atomic Bomb Radiatiom 

— ■ — Tota I (Ep i I at i on) 
— ■ — Pr i mary (Ep i I at i on) 
— ■ — Fa I I out (Ep i I at i on) 
— • — Total (Purpura) 
— • — Primary (Purpura) 
— • — Fa I lout (Purpura) 

— a— Total (Diarrhea) 
— * — Primary (Diarrhea) 
— A — Fa I lout (Diarrhea) 

Primary Radiation (DS02) 



3.0 



2.5 



> 

CD 



CD 
CO 
O 
Q 

"D 
CD 
CO 
O 

o. 

X 



2.0 



I 

-f — 

\ 
\- 




1.5 



1.0 



0.5 



0.0 

01 23456789 10 11 12 
distance from hypocenter km 

Figure 9.10 - Exposure to the Nagasaki bomb radiation 

The peak values of fallout radiation dose is, about 1.4 Gy at 1.7 km for epilation 1.6 
~ 1.7Gy at 2.0 km for purpura and diarrhea, respectively. It should be noticed here 
that the fallout exposed dose decrease until about 5 km from the ground zero but 



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ECRR Proceedings Lesvos 2009 

then become flat with constant values about 1.2~1.3 Gy which continue toward 
examined distance about 12 km. 

On the basis of the dose-incident rate relations given, I analyze the combined data of 
incidence rates of acute diseases and obtained the results summarized in Figure 12. 
The full lines with closed circles, open squares and triangles are corresponded to the 
estimated doses from the incident rate of epilation, purpura and diarrhea, 
respectively. As shown the obtained exposure dose F(r) from fallout exceed those of 
from the primary radiation cP(r) in the region more distant 1.2 km from the 
hypocenter. The peak values of fallout radiation dose F(r) about 0.8 Gy at 1.3 km, 
0.95 Gy at 1.7 km and 0.8 Gy at 2.0 km for epilation, purpura and diarrhea, 
respectively. It should be noticed here that the F(r) decrease until about 5 km from 
the hypocenter but then become flat with constant values about 0.5 Gy which 
continue toward examined distance about 12 km. 



Entrant Survivor's Incident Re 



Exposure of Entrant Survivors 
from Incident Rate of Acute Diseases 



Acute Diseases Rate 
■ Incident Rate of Depilatio 
* Incident Rate of PurPura 
A Incident Rate of Diarrhea 

Acute Diseases Fit 

-^--Dcpilation Fit 

-->-- Purpura Fit 

--^- -Diarrhea Fit 

^SiIq 




2.0 



1.5 



0.5 



0.0 



1 


07 (V 




-Any Acurate 




* 




— 1 — uupj JdLIUII 

—•—Purpura 
" — *— Diarrhea 
" — <s — external exposure dose (Okm) 

-^--external exposure dose(0. 5km) 

...J. 1 J. . Ml. .\ 
































llli 
































! ! ! ! 
























] 










1 






l : T : : : 




















flifpocefiter "" t * 
A^jutuI ated Exjter 




T 




twit— — -j---^-*^----— -t-*^ 






«H»YW i ■ i i i i i i i i i ■ ■ ■ i i i i i ■ i i i ■ ■ i ■ ■ ■ 





5 10 15 20 25 30 35 

Entrant Days after the Explosion (Day; 



5 10 15 20 25 30 35 

Enterid Day (After Explosion) 



Figure 9.11 - Entrant survivor exposures 



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ECRR Proceedings Lesvos 2009 

10 

Risk assessment of radiation-induced stomach cancer in 
the population of Belarus 

Prof. M.V. Malko 

Institute of Power Engineering, National Academy of Sciences of Belarus, Minsk, 
Belarus 

Abstract 

Results of analysis of the incidence in stomach cancers in the Belarusian population 
are described in the present report. They were established by using a modified 
ecological method based on the analysis of temporal patterns of the crude incidence 
in stomach cancers in different regions of Belarus in 1970-2006. It was found that 
approximately 2047 additional stomach cancers appeared in Belarus in 1991-2001 
(95% CI from 1,472 to 2,630 cases). The number of stomach cancers registered in 
Belarus in this period is about 42,587 cases (40,540 expected cases). 

The performed analysis shows that the numbers of additional stomach 
cancers manifested in different regions of Belarus are proportional to collective 
equivalent doses of the whole body irradiation delivered as a result of the Chernobyl 
accident and the relative risk, RR, is a linear function of the population dose of the 
whole body irradiation caused by this accident. These findings indicate that 
additional stomach cancers manifested in regions of Belarus after the accident at the 
Chernobyl NPP .were caused by radiation. 

Assuming radiation origin of additional stomach cancers time-averaged 
radiation risks were assessed for the period 1991-2001 in the report. According to 
assessment the relative risk, RR, estimated for the entire Belarusian population is 
1.050 (95% CI from 1.036 to 1.065). The excessive absolute risk of stomach 
cancers, EAR, averaged for this period is assessed as 85 cases per 10 4 PYSv (95% 
CI from 60 cases to 1 10 cases per 10 4 PYSv). The averaged excessive relative risk, 
ERR, is estimated equal to 2.4% per 1 mSv (95% CI from 1.7 to 3.1% per 1 mSv) 
and the averaged attributive risk, AR, is assessed equal to 5.0% (95% CI from 3.6 to 
6.5%). 



Introduction. 

The accident at the Chernobyl NPP caused a quasi-acute irradiation of the thyroid 
gland and a long-term irradiation of the whole body of affected populations. 



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ECRR Proceedings Lesvos 2009 

According to assessment [1] the collective equivalent dose of the thyroid gland 
irradiation delivered as a result of the Chernobyl accident to the Belarusian 
population could reach 1.3 Million PGy. This gives the population dose of the 
thyroid gland irradiation of the entire Belarusian population equal to 130 mGy. This 
is comparable with arithmetic mean dose of the thyroid gland irradiation of atomic 
bomb survivors [2]. Individual thyroid doses of the Belarusian children exceeded in 
some cases 60 Gy [3]. Doses of the whole body irradiation of the Belarusian 
population are much less than doses of the thyroid gland irradiation. For 
comparison, the highest dose of the whole body irradiation in Belarus is not higher 
than 1,500 mSv [4]. This is by factor 40 less than the maximal dose of the thyroid 
gland irradiation in Belarus. The same relation exists between the collective 
equivalent doses of the thyroid gland and the whole body irradiation in Belarus as 
well as in other affected countries including Ukraine and Russia. 

High doses of the thyroid gland irradiation caused in Belarus manifestation 
of radiation-induced thyroid cancers already some years after the Chernobyl 
accident [5-7]. 

Reliable data found by Russian, Belarusian and Ukrainian specialists for 
liquidators and people living in areas with high level of contamination demonstrate 
also manifestation of medical effects other than radiation-induced thyroid cancers 
among populations affected as a result of the Chernobyl accident. 

In case of Belarusian liquidators a statistical reliable manifestation of 
radiation-induced thyroid, urinary bladder, lung and stomach cancers has been 
established [8]. The similar findings were also established for Russian and Ukrainian 
liquidators [9-13]. 

Manifestation of radiation-induced malignant neoplasms among Belarusian, 
Russian and Ukrainian liquidators can be considered as some indirect evidence of 
manifestation of radiation-induced cancers also among inhabitants of contaminated 
regions of Belarus, Russia and Ukraine because radiation risk of this category of 
affected people has to be even higher than radiation risk of liquidators. It is well 
known that only healthy young people that had no some chronic diseases were 
employed at the mitigation of the Chernobyl accident consequences [10]. Their 
mean age was approximately 30 years at the moment of involving in mitigation of 
Chernobyl consequences. Practically all liquidators were males (approximately 
97%). This specific of liquidators indicates that their radiation risk can be different 
from radiation risk of general population that is heterogeneous in respect of 
carcinogenic impact of ionizing radiation, has different age distribution and has not 
only external irradiation but a comparable internal irradiation as a result of 
consumption of contaminated food staffs and drinking water. 

The mentioned assumption about the possibility of radiation-induced 
cancers among affected populations other than liquidators of the Chernobyl accident 



145 



ECRR Proceedings Lesvos 2009 

is in full agreement with data established after this accident. Practically the same or 
even higher increase in the incidence of different malignant neoplasms was 
registered in high contamination regions of Belarus. In accordance with data 
established by author [14] relative risk of stomach, rectum, lung and urinary bladder 
of inhabitants of Mogilev oblast living in areas with the mean level of contamination 
with the isotope 137Cs from 555 to 1480 kBq/m 2 exceeded factor 2. 

Data of the report [14] are in a good agreement with results of studies [15- 
19]. 

To the most outstanding features of radiation cancers caused in affected 
population as a result of the Chernobyl accident belong very high coefficients of 
radiation risk. They are by many factors higher than coefficients of radiation risk 
established for atomic bomb survivors [15-19]. For example, the excessive relative 
risk of the incidence in stomach cancers in Belarus according to data of the report 
[16] is equal to 13.9/Sv. This value is approximately 40 times higher than the 
excessive relative risk of stomach cancers by atomic bomb survivors irradiated at the 
age 30 years [20]. Such significant disagreement contradicts with main principles of 
the radiation paradigm based on the assumption that radiation risk of long-term 
irradiation at low dose rates is by some factors less than radiation risk of acute 
irradiation. The main task of the present report is an assessment of radiation risk of 
stomach cancers by using empirical data established in longer follow up period than 
it was done in reports [14-16] in order to examine the correctness of conclusions 
made in these report about very significant disagreement in radiation risk of normal 
population and atomic bomb survivors. 

Materials and methods. 

Published data of the Belarusian Cancer Registry on the standardized and crude 
incidences of stomach cancers in mixed populations of regions of Belarus 
established for the period 1970-2006 were used in the present work [21-32]. 

Registration of malignant neoplasms in Belarus is obligatory and exists from 
1953 [32]. Information about the incidence as well as about the mortality from 
malignant neoplasms is collected and assessed in 10 oncological dispensaries and 2 
oncological centres of Belarus: Oncological Department of Grodno Regional 
Hospital and N.N.Alexandrov Research Institute for Oncology and Medical 
Radiology of the Ministry of Healtn Care of the Republic of Belarus (Minsk). The 
last centre is situated in Minsk and is responsible for collecting of the necessary 
information in the Minsk oblast (region). 

The system of data on malignant neoplasms collecting in Belarus improved 
significantly beginning from 1953 richening the modern level allowing correct 
assessment of malignant neoplasms. It is fully computerized and automatized. This 



146 



ECRR Proceedings Lesvos 2009 

allows direct flowing of information from oncological dispensaries and oncological 
centres to the Belarusian Cancer Registry that is responsible for a critical evaluation 
of registered information preparing annual collections about malignant neoplasms in 
Belarus. These collections are published annually from 1994. They consist 
information for the entire Belarus and for separate regions of the country including 
the capital of the country, the city Minsk. 

Belarus is the unitary state. In administrative respect it is divided into 6 
oblasts (regions). They are: Brest, Gomel, Grodno, Minsk, Mogilev and Vitebsk 
oblasts (regions). They are similar in size and in the number of inhabitants (from 1,2 
up to 1.5 Millions of people). The city Minsk is the capital of the country and at the 
same time it is a centre of the Minsk region. 

Each administrative of Belarus unit has at least one oncological dispensary 
and this allows covering the entire territory of Belarus. 

All solid cancers (carcinoma and sarcoma) as well as malignant neoplasms 
of hematopoietic and lymphatic tissues (leukaemia, lymphoma, multiple myeloma 
and mucosis fungoides [32] are registered and evaluated in Belarus including rare 
cancers. However the information about rare cancers is not included in annual 
collections of the Belarusian Cancer Registry. 

The indices on the morphological verification of cancer diagnoses are 
improving steadily in Belarus and as it is known this is the main criterion of its 
realibity. According the updated data, on the average, 92.5% of all cancer cases were 
morphologically verified in 2004 and 94.9 in 2006 [32]. In case of many significant 
primary sites such as stomach, rectum, female breast, cervix and corpus uteri, 
prostate gland, thyroid gland the morphological verification is almost 100%. 
Comparison of data on standardized incidences in different cancers shows that data 
established in Belarus are similar to data found in developed countries having cancer 
registries [21]. This is an indication of a high quality of data of the Belarusian 
Cancer Registry. 

The crude incidence rates of stomach cancers published by the Belarusian 
Cancer Registry were used in the present report for an assessment of observed and 
expected numbers of stomach cancers manifested after the accident at the Chernobyl 
NPP. The method of "window" was used for this purpose. This method is based on 
approximation of observed crude rates of the incidence in stomach cancers by 
excluding data registered in some defined period of time. The established 
approximation is used later for an assessment of expected incidences and expected 
numbers of stomach cancers in this period of time. Using expected numbers of 
stomach cancers estimated on a way allows assessing relative risk in the "window" 
period. The period from January 1 1991 to December 31 of 2001 was chosen as the 
"window" period because analysis of observed incidences in stomach cancers give 



147 



ECRR Proceedings Lesvos 2009 

an indication of manifestation of additional stomach cancers in regions of Belarus 
affected at the Chernobyl accident in this period. 

The time-averaged relative risk of the incidence in stomach cancers in the 
"window" period was assessed by formula: 






where and ]7 are numbers of observed and expected stomach 

cancers in this period. 

The expression (1) was used for an assessment of relative risk of the crude 
incidence in stomach cancers for all regions of Belarus as well as for the city Minsk. 

Excessive absolute and relative risks, EAR and ERR, as well as attributive 
risk, AR, were also assessed in the report. 

The excess absolute risk was assessed on the basis of the following 
expression: 






w pysv 



Here EjIR w " excess i ye absolute risk in the "window" period, 
N PYSv~ num b er of person-years-sievert accumulated in this period. 
The value of N PVSv i n the last expression is determined as: 



n 



-Coll 



N w pys v =ZH17 ■ 



f~1 If 

Here ff- - collective equivalent dose of the whole body 

irradiation in ith year of the "window" period and n number of years 
included in this period. 

The excess relative risk was assessed by using the formula: 



148 



ECRR Proceedings Lesvos 2009 



(OJE w )-i 



ERR w~ w w ' (4) 

N PYSv 1 N py 



rW . 



The value of TV P7 * s estimated by using the following formula: 



i-n 

Here J\{ • is a number of persons in ith year of the "window" period. 
The attributive risk, AR , was assessed on the basis of the expression: 

AR W = 100% \Ow_Ej 



Confidence intervals of time-averaged values of RR W , EARw" 

ERRw m ^ARw were a ^ so assesse( i i n ^e present report. Method of 
assessment is described in appendix of the present report. 

Time-averaged collective and population doses of the whole body 
irradiation used for an assessment of radiation risks were taken from the report [33]. 
They are given in Tables 1 and 2. 



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ECRR Proceedings Lesvos 2009 



Table 10.1. Collective and population doses of the whole body irradiation of 
populations of Belarus in 1986-2007 as a result of the Chernobyl [33]. 





Collective doses, 










Region, city 


person- 


sievert 




Population doses, 


mSv 




Mixed 


Males 


Females 


Mixed 


Males 


Females 


Brest 


1,873 


988 


885 


1.27 


1.43 


1.13 


Gomel 


9,702 


5,711 


3,991 


6.48 


8.11 


5.03 


Grodno 


901 


515 


386 


0.77 


0.93 


0.62 


Minsk 


3,694 


2,474 


1,220 


2.36 


3.37 


1.47 


Mogilev 


2,529 


1,502 


1,028 


2.05 


2.59 


1.57 


Vitebsk 


646 


421 


225 


0.46 


0.64 


0.31 


city Minsk 


1,705 


1,125 


580 


1.03 


1.44 


0.66 


Combined 


21,050 


12,736 


8,314 


2.11 


2.71 


1.57 



By assessment of data given in Table 1 all possible pathway of the whole 
body irradiation of the Belarusian population were considered. Data presented in 
Table 2 show contribution of these pathways to total doses. 



150 



ECRR Proceedings Lesvos 2009 

Table 10.2. Collective doses of the whole body irradiation of populations of the 
Belarusian regions in 1986-2007 as a result of the Chernobyl [33]. 



Region, city 



rrColl 
ti DD 



zjColl 
M ME 



TjColl 
M MI 



TjColl 
M Ev 



TjColl 



H 



Coll 
Lq 



TjColl 



Person-sievert 



Brest 


1,250 


-55 


96 





378 


204 


1,873 


Gomel 


6,030 


-350 


-500 


640 


1,711 


2,171 


9,702 


Grodno 


293.5 


-13 


62.5 





384 


174 


901 


Minsk 


303 


-14 


174 





1,837 


1,394 


3,694 


Mogilev 


942 


-103 


-196 





1,296 


590 


2,529 


Vitebsk 


6.5 





124.5 





295 


220 


646 


city Minsk 


200 


-20 


239 





676 


610 


1,705 



Combined 9025 



-555 



640 



6,577 



5,363 



21,050 



Here fff?/! - collective dose as a result of the whole body irradiation from 

deposited 

radionuclides (sum of external and internal irradiation doses; 

tt Coll - collective dose of the whole body irradiation related to migration 
H ME y * 

of people to 

countries of the world; 

r* n 
H MI ~ collective dose of the whole body irradiation related to migration 

from one 

oblast of Belarus to other; 

c~^ n 
H £ v - collective dose of the whole body irradiation of people evacuated in 

1986 from 

so-called 30-km zones of the Chernobyl NPP; 



151 



ECRR Proceedings Lesvos 2009 



r* 11 

H^q - collective dose of the whole body irradiation of people related to 

resettlements of 

inhabitants of contaminated areas of Belarus ; 

c^ 11 
H La " c °H ec tive dose of the whole body irradiation of liquidators; 

c^ ii 
H^ - combined collective dose of the whole body irradiation. 



As can be seen from data shown in Tables 1 and 2 the population of Vitebsk 
oblast accumulated lowest collective and population doses of the whole body 
irradiation caused by the Chernobyl accident. 



Results and discussions. 

The crude and standardized incidence rates in stomach cancers of the Belarusian 
population are the highest in Europe (excluding Russia and Ukraine). Tables 3-6 
present comparison of crude and standardized incidence rates of stomach cancers in 
1983-2008 observed in Belarus and in some countries of the North, Central, South 
and West Europe demonstrating this peculiarity of the Belarusian population. It can 
be considered as some indirect evidence that there was no underestimation of the 
incidence at least in stomach cancer in Belarus before the accident at the Chernobyl 
NPP. 

Data given in Tables 3-6 show that the crude and standardized incidence rates 
of stomach cancers in the Belarusian men and women were approximately 3-5 times 
higher in this period than in the Danish men and women. This difference was not so 
high in case of the former socialist countries (Slovakia, Slovenia) and the former 
European Soviet republics (Latvia). The reason of high incidence in stomach cancers 
of the Belarusian population is not known. Possibly this is a result of different diets 
in Belarus and other countries of Europe. 



152 



ECRR Proceedings Lesvos 2009 



Table 10.3. Crude incidence rates of stomach cancers in men in 1983-2008 [34-38] 



Country 


Time period 


1983-1987 


1988-1992 


1993-1997 


1998-2002 


2008 


Belarus 


47.8 


50.9 


47.8 


45.1 


44.9 


UK (England and 
Wales) 


27.8 


27.0 a 


- 


- 


- 


Denmark 


20.6 


15.0 


13.6 


11.9 


14.3 


Finland 


25,7 b 


22.6° 


18.8 


16.6 


14.0 


France (Doubs) 


18.9 


13.8 


13.7 


14.9 


- 


Italy (Biella Province) 


- 


- 


35.3 d 


33.5 


31.5 


Latvia 


39.6 


37.5 


36.2 


33.5 


33.1 


Slovakia 


36.3 


31.7 


27.8 


23.5 


20.8 


Slovenia 


32.l e 


31.4 


30.9 


30.2 


29.6 



Notice: a -1988-1990, b - 1982-1986, c - 1987-1992, d - 1995-1997, e - 1982-1987 



Table 10.4. Standardized incidence rates in stomach cancers in men in 1983-2008 
[34-38] 



Country 


Time period 


1983-1987 


1988-1992 


1993-1997 


1998-2002 


2008 


Belarus 


46.7 


46.8 


40.5 


35.7 


34.2 


UK (England and 
Wales) 


16.9 


16.l a 


- 


- 


- 


Denmark 


12.5 


9.0 


8.2 


7.1 


7.8 


Finland 


20.3 b 


16.6° 


12.6 


10.2 


7.3 


France (Doubs) 


15.1 


10.7 


9.5 


9.3 


- 


Italy (Biella Province) 


- 


- 


15.9 d 


14.5 


14.8 


Latvia 


34.1 


31.1 


28.2 


24.0 


21.7 


Slovakia 


31.7 


27.1 


23.5 


19.2 


15.3 


Slovenia 


e 

27.9 


27.0 


23.8 


20.9 


17.2 



Notice: a -1988-1990, b - 1982-1986, c - 1987-1992, d - 1995-1997, e - 1982-1987 



153 



ECRR Proceedings Lesvos 2009 



Table 10.5. Crude incidence rates of stomach cancers in women 1983-2008 [34-38] 



Country 


Time period 


1983-1987 


1988-1992 


1993-1997 


1998-2002 


2008 


Belarus 


31.1 


32.8 


30.0 


28.6 


29.1 


UK (England and 
Wales) 


17.0 


16.l a 


- 


- 


- 


Denmark 


13.2 


10.3 


7.9 


6.9 


7.7 


Finland 


22.4 b 


19.3° 


15.6 


13.1 


10.7 


France (Doubs) 


10.3 


7.9 


8.0 


7.6 


- 


Italy (Biella Province) 


- 


- 


26.4 


22.7 


20.8 


Latvia 


27.6 


25.0 


24.4 


25.5 


21.4 


Slovakia 


18.5 


16.2 


14.9 


13.8 


13.8 


Slovenia 


22.0 e 


19.4 


19.7 


18.3 


18.4 



Notice: a -1988-1990, b - 1982-1986, c - 1987-1992, d - 1995-1997, e - 1982-1987 



TablelO. 6. Standardized incidence rates in stomach cancers in women in 1983- 
2008 [34-38] 



Country 


Time period 


1983-1987 


1988-1992 


1993-1997 


1998-2002 


2008 


Belarus 


20.1 


20.1 


17.4 


15.3 


15 


UK (England and 
Wales) 


6.8 


6.3 a 


- 


- 


- 


Denmark 


5,7 


4.7 


3.6 


3.2 


3.6 


Finland 


b 

11.2 


9.2 C 


7.0 


5.6 


4.4 


France (Doubs) 


5.5 


3.7 


3.7 


3.4 


- 


Italy (Biella Province) 


- 


- 


8.1 d 


7.1 


7.7 


Latvia 


15,5 


13.0 


11.6 


14.1 


9.3 


Slovakia 


12.2 


10.3 


9.0 


7.8 


7.1 


Slovenia 


12.8 e 


10.6 


10.4 


8.8 


7.5 



Notice: a -1988-1990, b - 1982-1986, c - 1987-1992, d - 1995-1997, e - 1982-1987 



154 



ECRR Proceedings Lesvos 2009 

In qualitative respect the crude and standardized incidences of stomach 
cancers in men and women of Belarus are similar to crude and standardized 
incidences of this cancer in other European countries. At first it is to see from Tables 
3-6 that crude and standardized incidences in stomach cancers in the Belarusian men 
is approximately 1.5 times higher than in the Belarusian women as in case of other 
European countries. Secondly, it is to see that at least in the period 1983-2008 a 
permanent decrease of the crude and standardized incidences in stomach cancers 
occurred in Belarus as well in other European countries. 

Figure - 1 demonstrates crude incidence rates in stomach cancers in different 
regions (oblasts) of Belarus in 1970-2006 in comparison with the crude incidence 
registered in this period in Vitebsk oblast. The collective and population doses of the 
whole body irradiation of this oblast are much lower than respective values 
estimated for other regions of Belarus. This means that the possible manifestation of 
radiation-induced malignant neoplasms has to cause minimal influence on the 
spontaneous incidence in population of Vitebsk region. Therefore comparison of the 
incidence in stomach cancers observed in Vitebsk region and other regions of 
Belarus can demonstrate the possible impact of irradiation caused as a result of the 
Chernobyl accident. 

As can be seen from data shown in Figure -1 the incidence in stomach cancer 
in Vitebsk region was the highest in Belarus in the entire period 1970-2006. Only in 
case of Mogilev region crude incidence rates of stomach cancers are similar to crude 
incidence rates of this cancer in the Vitebsk population. 

The difference between incidence rates in stomach cancers in Vitebsk and 
other regions of Belarus was especially very high in the period before the accident at 
the Chernobyl NPP. For example, the time-averaged crude incidence rate of the 
incidence in stomach cancers in the city Minsk in 1970-1986 was by 1.7 times less 
than the time-averaged crude incidence rate of the incidence in stomach cancers in 
Vitebsk region estimated for the same period. In case of Brest oblast the time- 
averaged crude incidence rate of the incidence in stomach cancers in 1970-1986 was 
by 1 .4 times less than in Vitebsk region. 

The difference in the crude incidence rates of stomach cancers of the 
Belarusian regions is a result of the difference in age specific coefficient of the 
incidence in stomach cancers and the difference in age distribution of populations of 
different regions. This is demonstrated by data shown in Figure -2 and Figure -3. 

Figure -2 gives standardized incidence rates of stomach cancers in different 
regions of Belarus in 1970-2006 and Figure -3 shows fractions of people older than 
60 years in different regions of Belarus. 

As in case of crude incidence rates standardized incidence rates of the 
incidence in stomach cancers as well as fractions of people older than 60 years are 



155 



ECRR Proceedings Lesvos 2009 

given for different regions of Belarus in comparison with respective values 
estimated for population of Vitebsk region. 

Comparison of data presented in Figure -2 with data given in Figure -1 shows 
similarity of temporal patterns of standardized rates and crude rates of the incidence 
in stomach cancers for all regions of Belarus. This means that difference in age- 
specific coefficients of the incidence in stomach cancers in different regions before 
the accident at the Chernobyl NPP is a main reason of the difference in the observed 
crude incidence rates of stomach cancers in case of Brest, Gomel, Grodno and 
Minsk oblasts. 



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156 



ECRR Proceedings Lesvos 2009 



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157 



ECRR Proceedings Lesvos 2009 



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Figure 10.1 - Crude incidence rates of stomach cancers in mixed populations of 
different regions of Belarus in 1970-2006. 

Data given in Figure -2 demonstrate that standardized incidence rates in 
stomach cancers in populations of Vitebsk oblast, Mogilev oblasts and the city 
Minsk practically the same in the entire period 1970-2006. This is an indication that 
age-specific coefficients of the incidence in stomach caners in these regions of 
Belarus are practically equal in the entire period 1970-2010. Lower crude incidence 
rates in Mogilev oblast and the city Minsk in comparison with crude incidence rates 
of Vitebsk oblast are mostly result of difference in age distribution. Data shown in 
Figure -3 demonstrate that fractions of people at the age 60 years and older in 
Mogilev region and the city Minsk ale smaller than respective fractions of the 
Vitebsk population. 



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158 



ECRR Proceedings Lesvos 2009 



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159 



ECRR Proceedings Lesvos 2009 



50 

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Year 



Figure 10.2 - Standardized incidence rates of the incidence in stomach cancers in 
regions of Belarus. 

It is known that age is one of many factors of carcinogenic risk. Smaller 
values of fractions of people at the age 60 years and older at similar age-specific 
coefficients result in the lesser crude incidence rates of stomach cancers in Mogilev 
oblast and the city Minsk in comparison with Vitebsk oblast. 



160 



ECRR Proceedings Lesvos 2009 



u.^- 
















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In case of the city Minsk the low fractions of people at the age 60 years and 
older are main reasons for very significant difference in crude incidence rates of 



161 



ECRR Proceedings Lesvos 2009 

stomach cancers in comparison with Vitebsk region. Lower fractions of people at 
the age 60 years and older in Brest, Gomel? Grodno and Minsk regions contribute to 
lower values of crude incidence rates of stomach cancers in these regions of Belarus. 

Data presented in Figure -1 and 2 show that discussed difference in crude and 
standardized incidences in stomach cancers in regions of Belarus decreases after the 
accident at the Chernobyl NPP. This is especially clear in the case of Gomel oblast. 
In case of this region an increase in crude and standardized incidences in stomach 
cancers began approximately from 1990 with reaching some maximal values in 
1990-1995 and beginning of decrease after 1995 . These changes of temporal 
patterns of crude and standardized incidences in stomach cancers occurred in Gomel 
region practically in the period 1991-2001. Similar change of temporal patterns of 
crude and standardized incidences in stomach cancers occurred in other regions of 
Belarus though they were not so strongly pronounced as in case of Gomel region. 

No such change occurred in Vitebsk oblast that has the lowest collective and 
population doses. In case of Vitebsk region one can see practically linear decrease of 
crude and standardized incidences in stomach cancers in the entire period 1970- 
2006. 

Two different reasons can be responsible for mentioned change of temporal 
patterns of crude and standardized incidences in stomach cancers in Belarus. At first, 
this can reflect improved screening in stomach cancers after the accident. At second, 
this can reflect manifestation of additional or radiation-induced stomach cancers in 
regions of Belarus affected as a result of the Chernobyl accident. 

The difference in age-specific coefficients of the incidence in stomach cancers 
as well as difference in age study of possible reasons of discussed change in 
temporal patterns of the incidence in stomach cancers in regions of Belarus. This 
problem can be solved by using the method of "window" that is based on a study of 
temporal patterns of the crude incidence in stomach cancers in each separate region 
of Belarus. The period 1991-2001 was chosen in the present report as the "window". 
Table 7 shows approximations of the crude incidence in stomach cancers in all 
regions of Belarus developed by using of squire quadrat method by excluding 
incidence rates observed in the period 1991-2001. 



162 



ECRR Proceedings Lesvos 2009 



Table 10. 7. Approximation equation for assessment of expected incidence rates of 
the incidence in stomach cancers 



Region 


Equation 


R 2 


P 


Brest 


Y = 0.00867301 84-x 2 - 34.79018-x + 

+ 
34919.004 




p< 0.0001 


Gomel 


Y = 0.0070268989-x 2 - 28.236662-x + 

+ 
28399.869 


0.71492 


p< 0.0001 


Grodno 


Y = -0.199306-x + 423.4566 


0.64386 


p< 0.0010 


Minsk 


Y = -0.214101x + 468.1799 


0.55324 


p= 0.0036 


Mogilev 


Y = 0.0069764645-x 2 - 28.290633-x + 

+ 
28713.827 


0.872422 


p< 0.0001 


Vitebsk 


Y = - 0.486444-x + 1013.4898 


0.91493 


p< 0.0001 


city Minsk 


Y= 0.006603-X+ 16.831372 


0.00107 


p =0.9156 


Belarus 


Y = 0.0093634034-x 2 - 37.582179-x + 

+ 
37746.0774 


0.91892 


p< 0.0001 



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163 



ECRR Proceedings Lesvos 2009 



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Figure 10.3 - Fractions of persons at the age 60 years and older in regions of 
Belarus in 1970-2006. 

Figure 4 demonstrates crude incidence rates in stomach cancers in different regions 
of Belarus estimated by using approximations shown in Table 7 (expected incidence 
rates) as well as observed incidence rates in the period 1970-2006 



164 



ECRR Proceedings Lesvos 2009 



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166 



ECRR Proceedings Lesvos 2009 



44 

42 

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Belarus 




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Year 

Figure 10.5 - Expected and observed incidence rates of stomach cancers in regions 
of Belarus in 1970-2006. 

Table 8 gives expected and registered numbers of stomach cancers estimated 
for different regions of Belarus for the "window" period or for the period 1991- 
2001. The third row from below in this table presents data estimated by summing of 
respective data assessed for separate regions of Belarus. The last row of the Table 8 
gives data estimated for Belarus by using expected and observed incidence rates 
established for the entire country as an independent unit. 

Comparison shows a very good agreement of observed and expected stomach 
cancers estimated for the entire Belarus by using these two methods. For example, 
the deviation between observed numbers of stomach cancers is only 0.05% and 
deviation between expected numbers of stomach cancers is only 0.1%. The rounding 
of empirical data used by estimation of crude incidence rates is the reason of such 
deviation. However, the existence even such small deviations in expected and 
observed values reflects in some larger deviations in numbers of additional stomach 
cancers estimated in the present report for the entire Belarus (1,983 and 2,047 



167 



ECRR Proceedings Lesvos 2009 

cases). Assessment by using these values gives the deviation equal 3.1%. It is clear 
that such small deviation is practically insignificant for estimation of additional 
stomach cancers. On the contrary, it is reliable evidence that the "window method" 
allows describing of additional stomach cancers very correctly. 

Table 10.8. Incidence of stomach cancers in regions of Belarus in 1991-2001. 



Region 


Observed 


Expected 


O-E 


Brest 


5,455 


5,159 


296 


Gomel 


7,001 


6,062 


939 


Grodno 


4,739 


4,554 


185 


Minsk 


7,417 


7,084 


333 


Mogilev 


5,633 


5,491 


142 


Vitebsk 


6,675 


6,641 


34 


city-Minsk 


5,645 


5,591 


54 


Combined 


42,565 


40,582 


1,983 


Belarus 


42,587 


40,540 


2,047 



Table 9 presents values of relative risk of additional stomach cancers in 
different regions of Belarus and in the entire country assessed for the period 1991- 
2001. As can be seen from these table statistical reliable values of the relative risk 
were estimated only for Breast, Gomel and Minsk as well as for the entire Belarus. 
The highest value of the relative risk was established for the Gomel oblast that is the 
most affected region of Belarus. The other regions of Belarus for which reliable 
values of relative risk were found were also affected at the Chernobyl accident. 



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ECRR Proceedings Lesvos 2009 



Table 10.9. Relative risk of additional stomach cancers in regions of Belarus in 
1991-2001. 



Region 


RR 


95% CI of RR 


Brest 


1.057 


1.018 


1.098 


Gomel 


1.155 


1.116 


1.195 


Grodno 


1.041 


0.999 


1.084 


Minsk 


1.047 


1.013 


1.082 


Mogilev 


1.026 


0.988 


1.0651 


Vitebsk 


1.005 


0.972 


1.040 


city Minsk 


1.010 


0.973 


1.048 


Belarus 


1.050 


1.036 


1.065 



This fact allows to assume that radiation is the main reason for manifestation 
of additional stomach cancers manifested in regions of Belarus after the accident at 
the Chernobyl NPP. This conclusion is supported also by existing of linear 
dependence of relative risk on population dose and of the number of additional 
stomach cancers on the collective dose of the whole body irradiation. Such linear 
dependence is shown in Figure -5 and Figure -6. 



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ECRR Proceedings Lesvos 2009 



1.16- 
1.14- 
1.12- 

| 110 

1.08-1 

> 

1 1.06- 

o 

a 1.04- 
1.02 
1.00 



Gomel oblast ■ 



Brest oblast 
■ 
Grodno oblast 



Minsk oblast 



Mogilev oblast 



■ City Minsk 

Vitebsk oblast 

— i — i — i — i — i — 

1 2 



- r - 
4 



— r~ 
6 



Population dose, mSv/person 



Figure 10.5 - Time-averaged (1992-1001) relative risk of the incidence in stomach 
cancers in regions of Belarus. 



<D 

</) 
o 

c 
o 

< 



1000 
800 
600 
400 
200 




Gomel oblast 



Brest oblast 
■ 
Grodno oblast 



Minsk oblast 



Mogilev oblast 
i city Minsk 
Vitebsk oblast 



0.0 0.2 0.4 0.6 0.8 1.0 

Collective dose, person-sievert 



Figure 10.6 - Numbers of additional stomach cancers in regions of Belarus in 1991- 
2001. 



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ECRR Proceedings Lesvos 2009 



Using the least squire method gives the following equation for estimation of 
values of the time-averaged (1991-2001) relative risk of additional stomach cancers 
manifested in Belarus after the Chernobyl accident: 

RR w = 0.022S-h pop + l.OO, R 2 = 0.865, ^ = 0.0024, 

where fa is population dose expressed in millisieverts. 

Nadd = 952 • H w {Coll)- 3, R 2 = 0.919, /> = 0.00064- 



In case of additional stomach cancers the following approximation was 
established in the present report: 



N w = ^2-H w (Coll)-3, 



where J-f is the collective dose in the "window period" (1991-2001). 

Linear dependence of the relative risk on population dose as well as of the 
numbers of additional stomach cancers on collective dose of the whole body 
irradiation indicates that radiation is the main reason for observed change of 
temporal patterns of the crude incidence in stomach cancers observed in regions of 
Belarus after the accident at the Chernobyl NPPO. 

Coefficients of radiation risks as well as attributable risk of stomach cancers 
were evaluated in the present report assuming that the radiation origin of discussed 
change the. This was done by using data established for the entire Belarus in order to 
diminish the possible deviations of rounding. Results of this evaluation are presented 
in Table 10. 



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ECRR Proceedings Lesvos 2009 

Table 10.10 Assessment of radiation risks of stomach cancers in Belarus in 1991- 
2001 



]\f pY , person-years 


112,314,289 


^ , mSv/person 


2.11 


4 

Npysv / 1 ' person-year-sievert 


23.7 


Observed cancers, cases 


42,587 


Expected cancers, cases 


40,540 


Additional cancers, cases 


2,047 


RR 


1.050 


95% CI of RR 


from 1.032 to 1.072 


EAR/\Q 4 PYSV 


86.4 


95% CI of EAR 


from 11.1 to 161.6 


ERR , %/mSv 


2.4 


95% CI of ERR 


from 0.3 to 4,5 


AR , % 


5.1 


95%ofAR 


From 3.9 to 6.3 



Table 1 1 presents comparison of data on radiation risks of stomach cancers 
assessed in the present report and data established for atomic bomb survivors [20]. 

For comparison of values estimated in the present report and values 
established for atomic bomb survivors coefficients of radiation risks of stomach 
cancers in Belarus shown in Table 1 1 were expressed in units of absorbed dose by 
converting doses. This was done by dividing of population and collective doses of 
the whole body irradiation used be estimation of values presented in Table 10 0.7 
Sv/Gy because this factor was used by evaluation of respective doses in reports 
[1,4,33]. 

Data shown in Table 1 1 demonstrate significant disagreement in coefficients 
of radiation risks established in the present report and for atomic bomb survivors. It 
is especially very high in case of excessive relative risk. The value of excessive 
relative risk estimated in the present report (16.8/Gy) is by factor 49.4 times higher 
than the excessive relative risk found for atomic bomb survivors (0.34/Gy). 



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ECRR Proceedings Lesvos 2009 

Table 10.11. Comparison of radiation risks of the incidence in stomach cancers in 
the Belarusian population and in atomic bomb survivors. 



Sources 


This report 


Preston et al [20] 


Period 


1991-2001 


1958-1998 


TV py ' P erson_ y ears 


112,314,289 


2,764,732 


h P o P > mG y f v Qrson 


3.0 


100 


4 

NpYGy / 1 ' Person-year-grey 


33.8 


- 


Observed cancers, cases 


42,587 


4,730 


Expected cancers, cases 


40,540 


4,579 


Additional cancers, cases 


2,047 


151 


RR 


1.050 


1.033 


90% CI of RR 


From 1.039 to 1.063 


- 


EAR/\Q 4 PYGy 


60.6 


9.5 


90% CI of EAR 


From 44.1 to 104.7 


From 6.1 to 14 


ERR , %/Gy 


16.8 


0.34 


90% CI of ERR 


From 4.6 to 29.0 


From 0.22 to 0.47 


AR , % 


5.1 


7.2 


90%ofAR 


From 3.9 to 6.3 


- 



In case of the excessive absolute risk such ratio is 6.3 or by factor 7.8 less than 
ratio of excessive relative risks. Such big difference of ratios of excessive relative 
risks and excessive absolute risks is a clear evidence of difference in the crude 
incidences in stomach cancers. In case if compared population have equal crude 
incidences in cancers ratios of excessive relative risk and excessive absolute risk 
have to be the same. Conclusion about difference in incidences in stomach cancers 
of the Belarusian and Japanese population is supported by comparison of data 
presented in Table 12 with data given in Tables 3-6. 



Table 10.12. Crude and standardized (World standard) incidence rates of stomach 
cancers in men and women of Hiroshima prefecture (Japan) [34-37] 



Period 


Men 


Women 


Crude 


Standardized 


Crude 


Standardized 


1978-1980 


74.0 


79.9 


41.0 


35.8 


1981-1985 


88.9 


85.8 


49.0 


38.9 


1986-1990 


95.7 


83.1 


51.1 


35.9 


1991-1995 


113.1 


85.5 


55.1 


33.9 


1996-2000 


123.8 


80.3 


57.1 


30.2 



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ECRR Proceedings Lesvos 2009 



As can be seen from these data crude and standardized incidences in stomach 
cancers in men and women of Belarus are by some factors less than in men and 
women of the Hiroshima Prefecture. 

Dependence of the excessive relative risk from the background incidence in 
cancers requires a special adjustment of relative risk by considering the difference in 
background incidence in cancers. Simple comparison of excessive relative risks 
estimated for different population without such adjustment can cause incorrect 
conclusions about carcinogenic impact of ionizing radiation. In case of data 
estimated in the present report it were fully unjustified to say that data of this report 
indicate that radiation risk of stomach cancer is by factor 49.4 higher than radiation 
risk established for atomic bomb survivors. 

In reality results established in the present report allow only to conclude that 
radiation risk of long-term irradiation of the Belarusian population is only by factor 
6 higher than radiation risk found for atomic bomb survivors. 

Discussed features of relative and absolute radiation risks show that absolute 
risk gives more direct evidence of carcinogenic impact of ionizing radiation and this 
indicates that collective dose of irradiation is useful instrument by assessment of 
health consequences of some large radiation accident like the accident at the 
Chernobyl NPP. 

It is clear that this six fold difference in radiation risk of stomach cancer can 
not be explained as a result of six fold underestimation of the whale body dose 
irradiation of the Belarusian population or as a result of six fold underestimation of 
numbers of additional stomach cancers established in the present report for the 
period 1991-2001. A number of other reasons can be responsible for discussed 
difference of radiation risks. 

Firstly this difference can be result of damage of the thyroid gland of the 
Belarusian population received very high doses of the thyroid gland irradiation. It is 
well known that there is a very tight link between endocrine, heurohumoral and 
immune systems. The damage of every of these systems has reflects in distortions in 
functioning of other related systems. 

Secondly, the difference in radiation risks can reflects higher carcinogenic 
impact of long-term irradiation in comparison with an acute irradiation. In case of 
acute irradiation only small fractions of cells is in the stage of preparing for dividing 
or undergo the process of dividing. All cells are very sensitive to impact of ionizing 



174 



ECRR Proceedings Lesvos 2009 

radiation in this stage. In case of long-term chronic irradiation significant fraction of 
cells in the high sensitive stage is irradiated. 

Thirdly, the difference in radiation risk can reflects some unknown effect of 
low doses and low dose rates of ionizing radiation. The accident at the Chernobyl 
NPP caused a quasi acute (some months) irradiation at quite high doses of the 
thyroid gland and long-term irradiation (many years) of the whole body in case of 
the affected Belarusian population. On the contrary, irradiation of atomic bomb 
survivors follows only some seconds [39]. 

Fourthly, ionizing radiation that affected the Belarusian population as a result 
of the Chernobyl accident was much softer than radiation of atomic explosions in 
Hiroshima and Nagasaki and this can contribute to difference in radiation risks of 
the affected Belarusian population and atomic bomb survivors. 

Fifthly, it can be result of internal irradiation of stomach. In case of the 
Belarusian population external and internal irradiation of the whole body was 
comparable,. In case of atomic bomb survivors external irradiation caused 
practically 100% of irradiation dose [39]. 

All mentioned reasons as well as some other unknown reasons can contribute 
to disagreement in radiation risk. At present it is clear only that coefficients of 
radiation risk established for atomic bomb survivors are not relevant for an 
assessment of health effects in case of normal population irradiated at doses and 
dose rates like the affected Belarusian population. Using of data established for 
atomic bomb survivors for assessment of medical populations that have long-term 
irradiation will cause a significant underestimation of possible medical effects of 
irradiation. This underestimation increases additionally if so-called DREFF factor 
(Dose and Dose Rate Effectiveness Factor) suggested by UNSCEAR, BEIR VII and 
ICPR are used for assessment of radiation effects [40-42]. According to the 
UNSCERA [40] the value of DDREF for solid cancers is from 2 to 10. BEIR VII 
recommends for solid cancers the value of DDREFF equal 1.5 [41]. 

Using the value of the excessive absolute risk of the incidence in stomach 
cancers established for atomic bomb survivors (9.5 cases per 10 4 PYGy, see Table 
11) and the value of DDREF factor recommended by BEIR VII) gives 262 
additional stomach cancers in Belarus for the period 1991-2001. This is by factor 7.8 
less than the number of additional stomach cancers assessed in the present report 
(2,047 cases). Using of the excessive relative risk found for atomic bomb survivors 
and the DDREFF factor equal 1.5 for assessment of radiation-induced stomach 



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ECRR Proceedings Lesvos 2009 

cancers in Belarus in 1991-2001 gives only 28 cases. That is by 73 times less than 
estimated in the present report. 

This assessment show that using data estimated for atomic bomb survivors 
together with the DDREFF factor underestimates significantly real health effects of 
radiation accidents and do not allow elaboration of adequate countermeasures for 
minimizing of their consequences. It was shown in our previous report [43] a 
significant underestimation of Chernobyl health effects assessed by authors [44] that 
used radiation risk established for atomic bomb survivors together with the value of 
the DDREF factor proposed by BEIR VII [41]. In accordance with results estimated 
in report [44] only 218 additional solid cancers other than thyroid cancers and non- 
melanoma skin cancers for the period 1986-2005 and 1,666 additional cancers of the 
same type for the period 1986-2065 can be expected in Belarus as a result of the 
Chernobyl accident. It is clear correct assessment can be performed only on the basis 
of an analysis of the incidence in studied cancers in territories affected at accidents. 
Such analysis diminishes possible underestimation of health effects among affected 
population. Using the excessive absolute risks seems preferable by performing such 
assessment. And this indicates that collective dose of irradiation is a very useful tool 
by assessment of radiological accidents and especially accidents like the accident at 
the Chernobyl NPP when there is no possibility to assess correctly individual doses 
of irradiation of all persons affected by the accident. It is much easier to assess in 
such cases collective doses of irradiation and this requires using of coefficients of 
absolute risk. 

Conclusions. 

Results of the analysis of the crude and standardized incidence in stomach cancers in 
regions of Belarus demonstrate the possibility of the manifestation of the radiation- 
induced stomach cancers in Belarus as a result of the accident at the Chernobyl NPP. 
Established linear relation-ship between relative risk and population doses of the 
whole body irradiation as well as between numbers of additional stomach cancers 
and collective doses of the whole body irradiation is a strong argument supporting 
the conclusion that these additional stomach cancers have a radiation origin. 
Radiation risks assessed in the present report assuming the possible link between 
additional stomach cancers and radiation are by some factors higher than radiation 
risks estimated for atomic bomb survivors. A number of reasons can be responsible 
for this difference. Especially high disagreement was established in the present 



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ECRR Proceedings Lesvos 2009 



report for the excessive absolute risk. This is an indication that using of excessive 
absolute risk is preferable in case of an assessment of health effects of radiological 
accident of large scale like the accident at the Chernobyl NPP. 

Existence of significant disagreement in radiation risks of thee Belarusian 
population and atomic bomb survivors demonstrate that using of radiation risks 
established for survived inhabitants of Hiroshima and Nagasaki underestimates real 
medical effects of the Chernobyl accident manifested at least in Belarus. This 
underestimation increases by using of the so-called Dose and Dose Rate 
Effectiveness Factor (DDREF) proposed by UNSCEAR, BEIR and ICPR. This 
means that radiation risks found for atomic bomb survivors and the idea of DDREFF 
using are not relevant at least in case of an assessment of radiation-induced stomach 
cancers caused in Belarus as a result of the Chernobyl accident. 



Appendix 

By assessment of the confidence interval of RR W ^ e s^pl^d method 

developed in the present report on the basis of the method of Katz et al [45] was 
used. Applying the method of Katz et al [45] gives for lower and upper limits of the 
confidence interval of relative risk RR w the following expressions: 



RR w {Upp) = e l 



(i) 



RR w (Low) = e 



w 



(2) 



Here the values V and W are determined by formulas: 



V = \0g e RR w + [Ni- a/ 2 >< SE^Og e RR w )\. 



(3) 



W = ^g e RR w - kl-a/2 >< SE ^g e RR w )\ 



(4) 



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ECRR Proceedings Lesvos 2009 



Here ff] -a / 2 * s ^ a PP ro P r i ate value from the standard Normal distribution for 
the 100(1 -a/2) percentile and S£|log RR W ) is standard error of 

log p RR w . 



sE{\og e RR w )= — \r + - \r (5) 

\j C/>v N py ^ w N py 



Introducing the value X : 



x = Ni- a/2 *s4og p RR w ) 



allows rewriting equations (3) and (4) in the form: 



(6) 



V = \og e RR w + 



X 



W = \0g e RR w -x. 



(7) 



(8) 



Inserting (7) and (8) into expressions (1) and (2) gives after some simple 
operations: 



RR w (Upp) = RR w -e x , ( 8) 



RR w (Low) = RR w - e x 



(9) 



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ECRR Proceedings Lesvos 2009 

It was found in the present report that for any region of Belarus as well as for 
the entire country the value of X is much less than 1. This allows using of the 
following approximations: 



? X « 1 + X 



(10) 



r x *i- x 



(ii) 



Using these approximations gives instead expressions (10) and (11): 



RR w (Upp)*RR w + xRR w . 



(12) 



and 



RR w (Low)*RR w -xRR w . 



(13) 



By inserting the value x determined by formula (6) expressions (13) and (14) 
can be written in the form: 



RRjUpp) * RR W + Ni-a/2 • Mog e #flJx RRw 



(14) 



RR w {u P p)*RR w -N l - a/2 [s4ogeRRwhRRw. 



(15) 



or in the form: 



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ECRR Proceedings Lesvos 2009 

RR w (Upp)* rr w + Ni- a /2 xSE (RR w )> (16) 

RR w (Low)*RR w -N l - a/ 2*S E (RRj (17) 

Here SE\J^R J is the standard error of the relative risk : RR : 



Se{rR w ) = SE(\ 0gp RR w )x RR W (18) 



By assessment of the confidence interval of the excessive absolute risk 
EAR w ^ e f°U° w i n g expression were used: 



EAR w (Up P )* EAR W + Ni- a /2 xSE (EAR w l (19) 

where SE\J7j[R J is the standardized error of EAR. It can be assessed by using 
the formula: 



se(ear w )= s(earJ- ear w (20) 

Here ^\EARw) * s ^ e re l a ^ ve error of the excessive absolute risk. It is 
determined by formula: 



s(EAR w ) = Ao w - E w )+ ?>(Npysv\ 



(21) 



180 



ECRR Proceedings Lesvos 2009 

where 5u) ~ E w) * s ^ e re l a ^ ve error of the value \0 W ~ E w ) anc * 

sfev) 

is the relative error of the collective dose of the whole body irradiation. The last 
value was taken equal to 30%. This is accuracy of population and collective doses of 
the whole body irradiation of the Belarusian population affected at the Chernobyl 
NPP accident [q,4,33]. 

Similar method was used also for estimation of confidence intervals of the 
excessive relative risk and the attributive risk. 

References 

1. Malko M.V. Assessment of the Chernobyl radiological consequences. In the 
report: Research activities about radiological consequences of the Chernobyl 
NPS accident and social activities to assist the sufferers by the accident. 
Edited by Imanaka T. Research Reactor Institute. Kyoto University, Japan. 
KURRI-KR-21. ISSN 1342-0852, 1998, p.65-85. 

2. Pierce D.A., Shimizu Yu., Preston D.L. et al. Studies of the Mortality of 
Atomic Bomb Survivors. Report 12. Part 1. Cancer: 1950-1990. Radiat. 
Res.l996,v. 146,p.l-27. 

3. Gavrilin Yu. I., Khrouch V.T., Shinkarev S.M. et al. Chernobyl accident: 
reconstruction of thyroid dose for inhabitants of the Republic of Belarus. 
Health Phys. February 1999, v.76, JV<>2, p. 105-1 19. 

4. Malko M.V. Doses of the whole body irradiation in Belarus as a result of the 
Chernobyl accident. In the report: Many-sided approach to the reality of the 
Chernobyl NPP accident - Summing up of the consequences of the accident 
twenty years after (II). Edited by Imanaka T. Research Reactor Institute. 
Kyoto University, Japan. KURRI-KR-139. ISSN, May 2008, p.136-146. 

5. Kazakov V.S., Demidchik E.P., Astakhova L.N. Thyroid Cancer after 
Chernobyl. Nature, 1992, v.359, p.359-360. 

6. Demidchik E.P., Drobyshevskaya I.M., Cherstvoy E.D. et al. Thyroid cancer 
in children in Belarus. In: Proceedings of the first international conference 
«The radiological consequences of the Chernobyl accident» held in Minsk, 
Belarus, in 1996 from 18 to 22 March. Edited by A.Karaoglou, G.Desmet, 
G.N.Kelly and H.G.Menzel. EUR 16544 EN. Brussels-Luxembourg. 1996, 
p.677-682. 

7. Demidchik E.P., Demidchik Yu.E., Gedrevich Z.E. et al. Thyroid cancer in 
Belarus. Int. Congr. Ser. 1234, 2002, p. 69-75. 

8. Okeanov A.E., Sosnovskaya E.Y., Priatkina O.P. A national cancer registry 
to assess trends after the Chernobyl accident. Swiss Med. Wkly. 2004; 
134:645-649. 

9. Ivanov V.K., Tsyb A.F., Maksyutov M.A. et al. Radiation and 
epidemiological analyses of data on participants of liquidation of 



181 



ECRR Proceedings Lesvos 2009 



consequences of the accident at the Chernobyl NPP included in the Russian 
State Medical and Dosimetric Register. Atomnaya Energia. M., v. 78, N2, 
1995, p. 121-127 (in Russian). 

10. Ivanov V.K., Rastopchin E.M., Gorsky A.I. et al. Cancer incidence among 
liquidators of the Chernobyl accident: solid tumors, 1986-1995. Health 
Phys. 1998, v.74, N3, p.309-315. 

11. Ivanov V.K., Tsyb A.F., Gorsky et al. Cancer Morbidity and Mortality 
among Chernobyl Emergency Workers: Estimation of Radiation Risks 
(1986-1995). Radiatsionnaya Biologiya i Ecologiya. M. 2006, v.46, p.159- 
166 (in Russian). 

12. Ivanov V.K., Tsyb A.F., Gorsky et al. Cancer Morbidity and Mortality 
among Chernobyl Emergency Workers: Estimation of Radiation Risks 
(1986-1995). Radiatsionnaya Biologiya i Ecologiya. M. 2006, v.46, p.159- 
166 (in Russian). 

13. Bebeshko V.G., Bobyliova O.A. Medical consequences of the Chernobyl 
nuclear Power Plant accident: experience of 15-years studies. Int. Congr. 
Ser. 1234, 2002, p. 267-279. 

14. Sosnovskaya E.Ya. Incidence of malignant tumors in Mogilev region the 
Chernobyl accident. Accomplishments of Medical Science in Belarus 
(Dostizheniya medicinskoy nauki Belarusi), 6 th Issue, Minsk: Belarusian 
Centre of Scientific Medical Information, 2001, p. 68 (in Russian). 

15. Malko M. Assessment of radiation-induced malignant neoplasms in Belarus. 
Proceedings of Fifth International Symposium and Exhibition on 
Environmental Contamination in Central and Eastern Europe. 12-14 
September 2000. Prague, Czech Republic. DOE Document Number: 
DOE/EM-0584, www.em.doe.gov 

16. Malko M.V. Risk assessment of radiation-induced stomach cancer in 
population of Belarus. In: Proceedings of the 3 rd Congress on Radiation 
Research (radiobiology and radiology). Kiev, 21-23 May 2003. The 
Ukrainian Radiobiological Society, The Kiev Taras Shevchenko 
University... Kiev, 2003, p. 408 (in Russian). 

17. Malko M.V. Risk assessment of radiation-induced lung cancer in population 
of Belarus. In: Proceedings of the 3 rd Congress on Radiation Research 
(radiobiology and radiology). Kiev, 21-23 May 2003. The Ukrainian 
Radiobiological Society, The Kiev Taras Shevchenko University ... Kiev, 
2003, p. 409 (in Russian). 

18. Malko M.V. Risk assessment of radiation-induced female breast cancer in 
population of Belarus. In: Proceedings of the 3 rd Congress on Radiation 
Research (radiobiology and radiology). Kiev, 21-23 May 2003. The 
Ukrainian Radiobiological Society, The Kiev Taras Shevchenko 
University. . . Kiev, 2003, p. 410 (in Russian). 

19. Malko M.V. Risk assessment of radiation-induced thyroid cancer in 
population of Belarus. In: Proceedings of the 3 rd Congress on Radiation 
Research (radiobiology and radiology). Kiev, 21-23 May 2003. The 
Ukrainian Radiobiological Society, The Kiev Taras Shevchenko 
University. . . Kiev, 2003, p. 41 1 (in Russian). 



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20. Preston D.L., Ron E., Tokuoka S. et al. Solid cancer incidence in atomic 
bomb survivors: 1958-1998. Radiat. Res. 2007, v. 168, p. 1-64. 

21. Zalutsky I.V., Averkin Yu. I., Artemova N.A., Mashevski A.A. 
Epidemiology of Malignant neoplasms in Belarus. Minsk, printed by "Zorny 
Shliach", 2006 (in Russian). 

22. Malignant Neoplasms in Belarus: 1987-1996. Ministry of Health Care of 
the Republic of Belarus. Belarusian Center of Medical Technologies, 
Information, Management and Economic of Health Care. Minsk, 1997. 

23. Malignant Neoplasms in Belarus: 1988-1997. Ministry of Health Care of 
the Republic of Belarus. Belarusian Center of Medical Technologies, 
Information, Management and Economic of Health Care. Minsk, 1998. 

24. Malignant Neoplasms in Belarus: 1989-1998. Ministry of Health Care of 
the Republic of Belarus. Belarusian Center of Medical Technologies, 
Information, Management and Economic of Health Care. Minsk, 1999. 

25. Malignant Neoplasms in Belarus: 1990-1999. Ministry of Health Care of 
the Republic of Belarus. Belarusian Center of Medical Technologies, 
Information, Management and Economic of Health Care. Minsk, 2000. 

26. Malignant Neoplasms in Belarus: 1991-2000. Ministry of Health Care of 
the Republic of Belarus. Belarusian Center of Medical Technologies, 
Information, Management and Economic of Health Care. Minsk, 2001. 

27. Malignant Neoplasms in Belarus: 1992-2001. Ministry of Health Care of 
the Republic of Belarus. Belarusian Center of Medical Technologies, 
Information, Management and Economic of Health Care. Minsk, 2002. 

28. Malignant Neoplasms in Belarus: 1993-2002. Ministry of Health Care of 
the Republic of Belarus. Belarusian Center of Medical Technologies, 
Information, Management and Economic of Health Care. Minsk, 2003. 

29. Malignant Neoplasms in Belarus: 1994-2003. Ministry of Health Care of 
the Republic of Belarus. Belarusian Center of Medical Technologies, 
Information, Management and Economic of Health Care. Minsk, 2004. 

30. Malignant Neoplasms in Belarus: 1995-2004. Ministry of Health Care of 
the Republic of Belarus. Belarusian Center of Medical Technologies, 
Information, Management and Economic of Health Care. Minsk, 2005. 

3 1 . Malignant Neoplasms in Belarus: 1 996-2005. Ministry of Health Care of 
the Republic of Belarus. Belarusian Center of Medical Technologies, 
Information, Management and Economic of Health Care. Minsk, 2006. 

32. Malignant Neoplasms in Belarus: 1997-2006. Ministry of Health Care of 
the Republic of Belarus. Belarusian Center of Medical Technologies, 
Information, Management and Economic of Health Care. Minsk, 2007. 

33. Malko M.V. Assessment of collective and population doses of the whole 
body irradiation of populations of regions of Belarus. In: Materials of the VI 
International conference "Medico-Social Ecology of Individual: Status and 
Perspective". 4-5 April 2008. Ministry of Education of the Republic of 
Belarus. Belarusian State University. Minsk, p. 175-177, 2008 (in Russian). 

34. International Agency for Research on Cancer. Cancer Incidence in Five 
continents. Vol. VI- Editers: Parkin D.M., Muir C.S., Whelan S.L., Gao Y.- 



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ECRR Proceedings Lesvos 2009 



T., Ferlay J., Powell J. IARC Scientific Publication No. 120. Lyon, France, 
1992. 

35. International Agency for Research on Cancer. Cancer Incidence in Five 
continents. Vol. VII- Editers: Parkin D.M., Whelan S.L., Ferlay J., 
Raymond L., and Young J. IARC Scientific Publication No. 143. Lyon, 
France, 1997. 

36. International Agency for Research on Cancer. Cancer Incidence in Five 
continents. Vol. VIII- Editers: Parkin D.M., Whelan S.L., Ferlay J., Teppo 
L., and Thomas D.B. IARC Scientific Publication No. 155. Lyon, France, 
2002. 

37. International Agency for Research on Cancer. Cancer Incidence in Five 
continents. Vol. IX- Editers: Curado M.P., Edwards B., Shin H., Ferlay J., 
Heanue M. and Boyle P. IARC Scientific Publication No. 160. Lyon, 
France, 2007. 

38. International Agency for Research on Cancer. GLOBOCAN 2008: Cancer 
Incidence and Mortality Worldwide. Editers: Ferlay J., Shin H., Forman D., 
Mathers C. and Parkin D.M. IARC CancerBase No. 10 [Internet]. 

39. Kerr G.D. et al. Transport of initial radiation in air over ground. Chapter 3, 
p. 66-142 in: U.S. - Japan reassessment of atomic bomb radiation dosimetry 
in Hiroshima and Nagasaki: Final Report. V.l. DS86 Dosimetry System 
1986. Edited by Roesch W.C. Hiroshima. RERF. 1987. 

40. United Nations. Sources, Effects and Risks of Ionizing Radiation. United 
Nations Scientific Committee on the Effects of Atomic Radiation. 1988 
Report to the General Assembly, with annexes. Annex D. Exposures from 
the Chernobyl accident. United Nations. New York. 1988, p.309-374. 

41. Committee to Assess Health Risks from Exposure to Low Levels of 
Ionizing Radiation. The USA National Research Council. Health Risks from 
Exposure to Low Levels of Ionizing Radiation: BEIR VII - Phase 2. ISBN: 
0-309-53040-7, National Academies Press, Washington, 2006. 

42. International Commission on Radiological Protection. Publication 60. 
Pergamon Press. Oxford. New York. Frankfurt. Seoul. Sydney. Tokyo. 
1991, p.108-111. 

43. Malko M.V. Assessment of Chernobyl Medical Consequences in European 
countries, www physiciansofchernobyl.org.ua/Docs/Malko/pdv. 

44. Cardis E., Krewski D., Boniol M., Drozdovitch V., Darby S., Gilbert E. et 
al. Estimates of the cancer burden Europe in from radioactive fallout from 
the Chernobyl accident. Int. J. Cancer, vol.1 19, pp.1224-1235, 2006. 

45. Katz D., Baptista J., Azen S.P. and Pice M.C. Obtaining Confidence 
Intervals for the Risk Ratio in Cohort Studies. Biometrics. Vol. 34, 
September 1978, pp. 469-474. Citated after Martin J. Gardner and Douglas 
G. Altman. Statistics with Confidence. Confidence intervals and statistical 
guidelines. British Medical Journal, 1989, pp. 51-52. 



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ECRR Proceedings Lesvos 2009 
11 

Risk assessment of radiation-induced thyroid cancer in 
population of Belarus 

Prof. M.V. Malko 

Institute of Power, National Academy of Sciences of Belarus, Minsk, Belarus 

The incidence in thyroid cancer in the Belarusian population are presented in the 
report. It was found that approximately 8,700 additional thyroid cancers occurred in 
Belarus in 1990-2006 The number of thyroid cancers registered in Belarus in this 
period is about 13,300 cases (4,600 expected cases). The relative risk averaged for 
this period is equal to 2.89 (95% CI from 2.80 to 2.99). The excessive absolute risk 
of thyroid cancer, EAR, averaged for the same period is assessed as 6.1 case per 104 
PYSv (95% CI from 5.8 cases to 6.4 cases per 104 PYSv). The averaged excessive 
relative risk, ERR, is found equal to 22.7/Sv (95% CI from 21.5 to 23.9/Sv) and the 
averaged attributive risk, AR, is estimated equal to 65.4% (95% CI from 62.1 to 
68.8%). The mean deposition level of iodine isotope 1311 on May 4, 1986 or one 
week after the accident at the Chernobyl Nuclear Power Plant was in some areas of 
the Gomel region higher than 37,000 kBq/m2. Recalculating with considering of the 
radioactive decay of this isotope gives the level of contamination higher than 74,000 
kBq/m2. Such high levels of contamination with the isotope caused very high doses 
of the thyroid gland among the Belarusian population. They were by some children 
higher than 50 Gy (50,000 mGy). The collective equivalent dose of the thyroid 
gland irradiation of the Belarusian population is about 1,000,000 PGy (assessment 
ofM.Malko). 

It is well known that thyroid cancer is a very rare disease by children. 
According to the data of Prof. Demidchic (Belarus) only 21 cases were registered 
among the Belarusian children (less than 15 years at the time of diagnose) in 1966- 
1985 or one case annually. This observed number of thyroid cancers in children 
corresponds to the number of person-years accumulated in the period 1966-1985 
equal to 4.74* 107. The last figure was assessed on the basis of demographic data 
given in handbooks of Belarus. Dividing the number of observed thyroid cancers 
among by this number of person-years gives the incidence rate of this cancers in 
children of Belarus equal to 0.443 cases per million persons-years. 



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ECRR Proceedings Lesvos 2009 



Country 


Time Period 


Crude 
rate 


Standardized rate 


Sources 


UK, England 
and Wales 


1981-1990 


0.6 


0.5 


IARC 


UK, England 
and Scottish 
Cancer 
Register 


1981-1990 


0.6 


0/5 


IARC 


Poland 


1980-1989 


0.5 


0.5 


IARC 


Slovakia 


1980-1989 


0.7 


0.6 


IARC 


Hungary 


1985-1990 


0.3 


0.3 


IARC 


Ukraine 


Before 

Chernobyl 

accident 


0.5 




Tronko 
et al 


Belarus 


1966-1985 


0.44 


- 


This 
report 



Table 11.1 - Time-averaged crude and standardized (World standard) incidences in 
thyroid cancers in children. 



Numbers of thyroid cancers registered in 

children of Belarus in 1986-2007 

(Data of Prof. E.Demidchic) 



100 




1985 1990 1995 2000 

Years 



2005 



2010 



Figure 11.1 - Thyroid cancer reporting 



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ECRR Proceedings Lesvos 2009 



Regions 


Observed 


Expected 


O-E 


RR 


Brest 


165 


3 


162 


55 


Vitebsk 


11 


2 


9 


5.5 


Gomel 


378 


3 


375 


126 


Grodno 


43 


2 


41 


21.5 


city Minsk 


62 


3 


59 


20.7 


region 
Minsk 


42 


3 


39 


14 


Mogilev 


43 


2 


41 


21.5 


Together 


744 


18 


726 


41.3 



Table 11.2 - Incidence in thyroid cancers in children ofBelarussian regions in 
1986-2004. 

Fractions of children irradiated in 1986 
as function of time 

120 



100 

80 

■2 60 
u 

LL 

40 
20 



H 



JZL 



N c? ^ ^ ^ ^ ^ ^ $> $> $> ^ ^ ^ ^ j§> j§> 

Years 



Figure 11.2 - As titled 



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ECRR Proceedings Lesvos 2009 




Years 



Figure 11.3 - Incidence rates of thyroid cancer among irradiated children of 

Belarus 



Number of thyroid cancers registered in 

adolescents of Belarus in 1986-2006 

(Data of Prof. E.P.Demidchic) 




2000 



2010 



Years 



Figure 11.4 -As titled 



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ECRR Proceedings Lesvos 2009 



Number of registered thyroid cancers in the 


cohort of persons that were at the age less than 


19 years at the Chernobyl NPP (Kenigsberg et al) 


Odf\ 






&OU 


♦ 




200 


♦ 




/ ^ 


Number of Cc 

m o ui 
o o o 


+-*/ 






♦ 


4 











1985 1990 1995 2000 2005 


Years 



Figure 11.5 - As titled 



Excessive relative risk (with 95% CI) of the incidence 

in thyroid cancer in Belarus in 1986-2002 in persons 

irradiated at the age 0-18 years 

(ERR =34.3/Gy in 1991-2002). 



60 

50 

40 

$ 30 

I 20 

10 





-10 





T 


^^""^^ VF^- 


; /l 1 L L ^ U 


]/ 


, J^i-Y 


yT~±^L 



1985 



1990 



1995 
Years 



2000 



2005 



Figure 11. 6- As titled 



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ECRR Proceedings Lesvos 2009 



Excessive absolute risk (with 95% CI) of the incidence 

in thyroid cancers in Belarus in 1986-2002 in persons 

irradiated at the age 0-18 years 

(EAR =2.7/10000 PYGy) 




1984 1986 1988 1990 1992 1994 1996 1998 2000 2002 2004 

Years 



Figure 11. 7 -As titled 



Incidence rates in thyroid cancers in population 
of Belarus in 1986-2007 




1985 



1990 



1995 



2000 



2005 



2010 



Years 



Figure 11.8 - As titled 



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ECRR Proceedings Lesvos 2009 



Age specific incidence rates in thyroid cancer in 
Belarus in 1991-2006 

■ 1991 ■ 1995 □ 2003 □ 2006 



30 
S 25 

a 20 

I 15 

.£ 10 



timlM 




\* & <p <£> op <%> p $ <J» <%> & <§> ^ ^> & oj> 
« n* f f # # P & <? <? ffi & ^ # $ « 



Figure 11.9 - As titled 



.5 



.4 



.3 



Incidence rates of thyroid cancers in males of 
Latvia in 1985-2005 (I ARC data) 

y = 0.0215X - 41.787 
R 2 = 0.9146 



1.1 



.8 A 
1980 



1985 1990 1995 
Year 



2000 



2005 



Figure 11.10- As titled 



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ECRR Proceedings Lesvos 2009 



Incidence rates in thyroid cancers in females of 
Latvia in 1985-2002 (I ARC data) 



5.5 



y = 0.1019X - 199.08 
R 2 = 0.9217 




1980 1985 1990 1995 

Year 



2000 



2005 



Figure 11.11 - As titled 



Incidence rates of thyroid cancers in the mixed 
population of Latvia in 1985-2002 (IARC data) 



4.5 



3.5 



2.5 



1.5 
1980 



y = 0.0646X - 126.08 



FT = 0.9166 



1985 1990 1995 2000 2005 
Years 



Figure 11.12 - As Titled 



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ECRR Proceedings Lesvos 2009 



Comparison of incidence rates in thyroid 
cancers in males of Latvia and Belarus 



c 
o 
(/> 

!- 

0) 

Q. 

o 
o 
o 
cT 

o 



-*— Latvia males 



Belarus males 



CO 

S 
O 



-I 
1985 



1990 1995 2000 2005 
Year 



2010 



Figure 11.13 - As titled 



Comparison of registered incidence rates in 
thyroid cancers in females of Latvia and Belarus 



- Latvia females 



Belarus females 



<D 

o 



20 

18 

16 

14 

12 

10 

8 

6 

4 

2 



1980 



1985 



1990 



1995 
Years 



2000 



2005 



2010 



Figure 11.14 - As titled 



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ECRR Proceedings Lesvos 2009 



Comparison of incidence rates of thyroid 
cancers in populations of Latvia and Belarus 



en 

c 
o 
en 

i- 
a> 

Q. 

O 

o 
o 
o 

o 



en 
a> 

s 

o 



12 

10 

8 

6 

4 

2 




1985 



— Pflfli 

P«fl2 



1990 



1995 2000 
Years 



2005 



2010 



Figure 11.15 -As Titled 



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ECRR Proceedings Lesvos 2009 





Belarus 


ATB* 


Period of time 


1990-2006 


1958-1998 


Contingent 


Males 


Females 


Mixed 


Mixed 


PY 


80,400,000 


91,300,000 


171,700,000 


2,764,731 


H(Coll), 10 4 PGy 


44 104 


50 104 




10 4 PGy 


h(population), 
Gy 


0.094 


0.094 


0.094 


-0.2 


Duration of 
irradiation 


2.6- 10 6 sec 


2.6- 10 6 sec 


2.6- 10 6 sec 


2.6 sec 


Dose rate, Gy/sec 


0.036- 10" 6 


0.036- 10" 6 


0.036- 10" 6 


0.1 


Observed 


1560 


10,800 


13,300 


471 


Expected 


2500 


3,660 


4,600 


408 


O-E 


940 


7,140 


8,700 


63 


RR 


2.66 


2.95 


2.89 


1.15 


95% CI of RR 


2.47-2.87 


2.83-3.06 


2.80-2.99 




EAR/10 4 PYGy, 


2.3 


9.3 


6.1 


1.2** 


95% CI of EAR 


2.1-2.6 


8.8-9.9 


5.8-6.4 


0.48-2.2 


ERR/Gy 


19.9 


23.3 


22.6 


0.57** 


95% CI of EAR 


17.6 22.4 


22 - 24.7 


21.5-23.7 


0.24- 1.1 


AR% 


62.4 


66.1 


65.4 




95%CIofAR,% 


59.5-65.1 


62.1-69.9 


64.2 - 66.6 





* D.L/Preston, E.Ron, S.Tokukoko et al. Solid Cancer Incidence in Atomic Bomb 
Survivors: 1958 - 1998. Radiation Research, vol.168, pp. 1-64 (2007). 

** Estimates for atomic bomb survivors irradiated at the age 30 years and attained 
age 70 years. 

Tablell. 3 - Comparison of radiation risks estimated for the Belarusian population 
and for atomic bomb survivors 

Conclusions 

The accident at the Chernobyl NPP caused in Belarus in 1990 - 2006 approximately 
8,700 radiation-induced thyroid cancers. The radiation risks of radiation-induced 
thyroid cancers caused in Belarus by the Chernobyl accident are by some factors 
higher than observed in atomic bomb survivors. The radiation risks of thyroid 
cancers established for atomic bomb survivors (acute irradiation) are not relevant for 
irradiation of normal population. Using radiation risks observed for the surviving 
inhabitants of Hiroshima and Nagasaki underestimates real number of radiation- 



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ECRR Proceedings Lesvos 2009 

induced thyroid cancers in case of a population exposed to chronic irradiation. Using 
the Dose and Dose Rate Effectiveness Factor higher than one additionally 
underestimates number of radiation-induced thyroid cancers caused as a result of a 
chronic irradiation of the normal population. 



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ECRR Proceedings Lesvos 2009 

12 

Tumours of hematopoietic and lymphoid tissues in 
Chernobyl clean-up workers 

D.F. Gluzman, L.M. Sklyarenko, V.A. Nadgornaya, M.P. Zavelevich, S.V. 
Koval 

R.E. Kavetsky Institute of Experimental Pathology, Oncology and Radiobiology, 
National Academy of Sciences of Ukraine, Kyiv, Ukraine 

The Chernobyl accident on April 26, 1986 remains the worst ever in the history of 
the nuclear industry. A dramatic increase in the incidence of thyroid cancer has been 
observed among those exposed to radioactive iodine in most contaminated areas. 
The question as to whether the incidence of leukaemias and malignant lymphomas 
among Chernobyl clean-up workers increased is still a point of much controversy. 
UN Scientific committee on effects of atomic radiation (report to UN General 
Assembly, 2001) and Chernobyl Forum (Vienna, 2005) reject the possibility of 
increasing leukaemia incidence in Chernobyl clean-up workers. Nevertheless, this 
point of view is inconsistent with the results of several descriptive epidemiologic 
studies in Ukraine, Byelorussia, and Russia. 

In 2006, the standardized incidence of leukaemia, lymphomas and multiple 
myeloma in adults amounted to 16.5 per 100,000 of population (crude data) 
(National Cancer Registry of Ukraine). The actual incidence rate is underestimated 
by about 30% since up to the day several categories of myeloproliferative diseases 
were not classified as "malignant neoplasms" in IDC- 10 (1992) and were not 
included in Ukrainian Cancer Registry. Various categories of MDS (refractory 
anemia with and without ringed sideroblasts, refractory cytopenia, refractory anemia 
with excess of blasts, 5q- syndrome) with total annual incidence of 3.0 per 100,000 
also were not accounted. We believe that only precise diagnosis of the major types 
of hematological malignancies among Chernobyl clean-up workers in comparison 
with the data in general population will be the basis for estimating the relative 
contribution of the radiation factor to the overall incidence of such pathologies. The 
conclusions of other authors are mostly based on crude data without delineation of 
the incidence according to the biological subtypes of leukaemia and lymphoma. The 
aim of the study is to present the data on the various forms and variants of leukaemia 
and lymphoma verified by Western standards in the consecutive group of 281 
Ukrainian Chernobyl clean-up workers developed in 10-23 years after Chernobyl 
accident, diagnosed in the Ukrainian Reference Laboratory in 1996-2008 and 



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ECRR Proceedings Lesvos 2009 

categorized according to the up-to-date classifications (FAB, WHO, EGIL, ICD-10, 
ICO-O-2). 



Bebeshko et al. (1999): 96 cases of leukaemia and MDS among clean-up 
workers enrolled in National Ukrainian Registry 

Ledoschuk et al. (2001): 71 cases of acute and chronic leukaemias, 59 
cases of malignant lymphomas, 15 cases of other myeloproliferative 
diseases (polycythemia vera, osteomyelofibrosis, MDS) 

Hatch et al. (2006): 87 cases of pathologically confirmed leukaemia 
(1986-2000) 

Kesmiene et al. (2008): 117 cases of neoplasms of lymphoid and 
hematopoietic tissue (69 leukaemia, 34 NHL, 8 multiple myeloma, 2 
MDS, 4 cases of myeloproliferative disease, unclassificable) in Belarus, 
Russian Federation, Baltic countries 

Cardis et al. (1996) estimated about 150 excessive cases of leukaemia 
within 10 years among 100,000 clean-up workers exposed to an average 
dose of 10 cSv 

Prisyazhniuk et al. (1999) stated statistically significant increment in 
observed-to-predicted ratio of leukaemia and lymphoma incidence: 2.6 
in 1990-1993 and 2.0 in 1994-1997 

Ivanov et al. (2003) diagnosed 58 cases of leukaemia in clean-up 
workers who received doses of 15-30 cGy (twofold increased risk has 
been shown in a very large cohort of clean-up workers in Russia) 

According to the forecasts of Russian scientists, for the cohort of clean- 
up workers with average dose of 16 cGy about 800 cases of leukaemia 
are expected, with 17% of cases being associated with radiation 
exposure (VK Ivanov, AF Tsyb et al.) 

Figure 12.1 - Summary of findings and estimations made by various research teams 
on leukaemia and lymphoma incidence in Chernobyl clean-up workers 



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ECRR Proceedings Lesvos 2009 



Year 


Number of clean-up workers 


Average dose in cGy 


1986- 
1987 


207,486 


18.5(14.4)* 


11.2(9.0)* 


1988-1989 


98,153 


4.7 (3.6)* 



Figure 12.2 - Cohort of Ukrainian clean-up workers - 305,639 persons (State 
Register) predominantly males aged 20-45 



Age groups at time of diagnosis: 

30-39 years- 12 pts. 
40-49 years - 39 pts. 
50-59 years - 89 pts. 
60-69 years- 107 pts. 
70 and above - 34 pts. 



Males: 240 

Females: 41 
Mean age: 62.4 ± 
1.6 



Neoplastic diseases of hematopoietic and lymphoid tissues: 281 pts. 

Non-malignant hematopoietic disorders (aplastic anemia, hemolytic anemia, 
idiopathic thrombocytopenia, neutrophylic leukocytosis, lymphocytosis, 
dysgranulocytopoiesis etc.) : 117 pts. 

Group of comparison: 2697 consecutive patients of general population 
diagnosed in 1996-2005 

Figure 12.3 - Chernobyl clean-up workers 1986-1987 



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ECRR Proceedings Lesvos 2009 



MGG staining of blood and bone marrow smears 

Cytochemical detection of myeloperoxidase, acid phosphatase, alkaline 
phosphatase, acid non-specific esterase, naphtol-AS-D-chloroacetate 
esterase, PAS reaction 

• Immunocytochemical detection of antigens (ABC-AP, APAAP methods): 

- Myeloid cells: CD33, CD13, CD15, CD64, CD16, MPO 

- Erythroid and megakaryocyte cells: CD 71, CD61, CD62, CD41, 
CD42, glycophorin A 

- T-cells: CD7, CD 5, CD3, CD2, CDla, CD4, CD8, CD45RO, 
ySTCR 

- B-cells: CD19, CD20, CD22, CD10, k, X, ju chains 

Stem cell and markers of commitation: CD34, CD38, CD45RA, 
HLA-DR 

Figure 12.4 - Diagnostic techniques 



Type of leukaemia 


Absolute number and relative frequency (percentage 
in the brackets) 


Chernobyl clean-up workers 


General population 


Myelodysplastic 
syndromes 


15 (5.34%) 


107 (3.70%) 


Acute myeloid 
leukaemia 


44(15.66%) 


732(27.14%) 


Acute lymphoblastic 
leukaemia 


17(6.03%) 


214(7.93%) 



Figure 12.5 - Summary of malignant diseases of hematopoietic and lymphoid tissues 
diagnosed in Chernobyl clean-up workers 



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ECRR Proceedings Lesvos 2009 



Chronic myelogenous leukaemia 


25 
(8.90%) 


178 
(6.59%) 


Polycythemia vera 


6(2.13%) 


3(0.11%) 


Essential thrombocythemia 


8 (2.85%) 


— 


Chronic eosinophylic leukaemia/ Hypereosinophylic 
syndrome 


2(0.71%) 




Chronic idiopatic myelofibrosis 


4(1.42%) 


2 (0.07%) 


Chronic myelomonocytic leukaemia 


8 (2.85%) 


84(3.11%) 


Chronic lymphocytic leukaemia 


75 
(26.96%) 


791 

(29.32%) 


B-cell prolymphocyte leukaemia 


4(1.42%) 


23 (0.85%) 


Hairy cell leukaemia 


11 
(3.91%) 


118 

(4.37%) 


Multiple myeloma 


18 
(6.41%) 


108 
(4.00%) 


Non-Hodgkin's lymphoma 
in leukemization phase 


34 
(12.13%) 


296 
(10.97%) 


Sezary syndrome 


3(1.07%) 


8 (0.29%) 


T-cell prolymphocyte leukaemia 


2 (0.71%) 


3(0.11%) 


Large granular lymphocytic leukaemia 


5(1.77%) 


3(0.11%) 



Figure 12.6 - Summary of malignant diseases of hematopoietic and lymphoid tissues 
diagnosed in Chernobyl clean-up workers 



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ECRR Proceedings Lesvos 2009 



All of B-Cell Origin: 

ALL with phenotype of stem hematopoietic cell: 
CD34 + , CD38 + , HLA-DR + , CD45RO + 
pre-pre-B-ALL: CD19 + , CD22 + , CD20 , CD 10 , cym" 
common ALL: CD 1 9 + , CD22 + , CD20 +/ ", CD 1 + , cym" 
pre-B-ALL: CD19 + , CD22 + , CD20 +/ , CD10 + , cym + 
B-ALL: CD19 + , CD22 + , CD20 + , CD10 + , slg + 





A 



&* 






^D 






• 






<Q> 






<*T 



'^§L 



& 



I 



Figure 12. 7 - PB smears in pre-B-cell ALL: 

a-MGGx900 

b - CD19 positive blast cells 

ALL of T-cell origin: 

Tl-ALL with a phenotype of subcortical thymocytes: CD7 + , CD2 + , cyCD3 + , 
CD5,CDla,CD4,CD8- 

T2-ALL with a phenotype of cortical thymocytes: 
CD7 + , CD2 + , sCD3 + , CD5 + CDla +/ ", CD4 + , CD8 + 

T3-ALL with a phenotype of medullar thymocytes: 
CD7 + , CD2 + , CD3 + , CD5 + , CDla + , CD4 + or CD8 + 



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ECRR Proceedings Lesvos 2009 



• T4-ALL with g8T-cell receptor: 

g8TCR + , CD7 + , cyCD3 + , CD2 + , CD5 , CD la , CD4 , CD8 

Immunophenotype of AML blasts 

MO-AML: HLA-DR + , CD34 + , CD33 + , CD13 + , MPO + 

Ml-AML: HLA-DR + , CD34 +/ , CD33 + , CD13 + , MPO + , CD15 + , CD64 + 

M2-AML: HLA-DR +/ , CD34 +/ , CD33 +/ , CD13 +/ , MPO + , CD15 + , CD64 + , 
CD16 + 

M3-AML: HLA-DR + Expression of pan-myeloid antigens varies 

M4-AML: Presence of myeloblasts and monoblasts 

M5-AML: Three stages of differentiation 

• AcNE^, CD14 ++ > CD15 +/_ 

• AcNE + , CD14 ++ , CD15 ++ 

• AcNE l0W , CD14 , CD15 + , cyHLA-DR + cyCD7 + 

• M6-AML: HLA-DR + , CD34 + , CD33 + , CD 1 3 + , CD7 1\ glycophorin A + 

• M7-AML: HLA-DR + , CD34 + , CD41 + , CD61 + 




Figure 12.8 - BMfilm of patient with acute megakaryoblastic leukaemia (M7AML): 

a-MGGx900 

b - CD41 positive blast cells 

c - CD61 positive blast cells 



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ECRR Proceedings Lesvos 2009 







e* 



Figure 12.9 - BMfilm of patient with acute hypergranular promyelocytic leukaemia 

(M3AML): 

a-MGGx900 

b - chloroacetate esterase stain showing a positivity in promyelocytes 

c - acid non-specific esterase stain showing a positivity in leukaemic cells 

It is worth notice that in seven AML patients (16% of all AML cases) leukaemia 
was preceded by MDS (including 2 patients with Ml AML, 2 - with M4 AML, 1 - 
with M4Eo AML; 2 - with M6 AML). At the same time, only 6 cases of preceding 
MDS were found upon examination of 373 AL patients in general population of 
Kyiv city and district (1.5%). 






Figure 12.10 - BMfilm in refractory anemia (a) an 

refractory anemia with excess of blasts (b,c): a, b-MGGx 900; 

c - myeloperoxidase stain showing negativity in majority of neutrophils and blasts 



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ECRR Proceedings Lesvos 2009 




Figure 12.11 - PBfllm in Chronic myelogenous leukaemia 

a-MGGx900 

b - positive peroxidase reaction 








Figure 12.12 - PBfilm in B-cell chronic lymphocytic leukaemia: 

a-MGGx900 

b - CD23-positive cells 



Advances in molecular biology and our understanding of the pathophysiology of B- 
CLL provide a strong basis for expecting that exposure to ionizing radiation may 
increase CLL risk. 



Richardson et al., 2005 
Silver et al., 2007 



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ECRR Proceedings Lesvos 2009 



Schubauer-Berigam et al., 2007 
Vryheid et al., 2008 
Hamblin, 2008 
Kesminiene et al., 2008 



According to our data, up-to-date B-CLL rate in Chernobyl clean-up workers 
(26.96%) is practically the same as in Ukrainian population in general (29.32%). 

Immunophenotypes of verified B-cell non-Hodgkin's lymphoma 

• Follicular lymphoma (10 pts.): CD19 + , CD20 + , CD22 + , CD10 +/ ", CD5", 
CD23 +/ ", CD25", CD43", CD lie" 

• Lymphoplasmacytic lymphoma (5 pts.): CD19 + , CD20 + , CD22 + , CD 10", 
CD5", CD23", CD25", CD38 + 

• Mantle cell lymphoma (5 pts.): HLA-DR + , CD19 + , CD20 + , CD22 + , CD5 + , 
CD23", CD 10", CyclinD + 

• Splenic marginal zone B-cell lymphoma (3 pts.): HLA-DR + , CD19 + , CD20 + , 
CD22 + , CD5", CD23", CD25", CD 10", CD43", slg + 

• Diffuse large B-cell lymphoma (8 pts.): CD19 + , CD20 + , CD22 + , CD79a + , 
CD5", CD23" 

Extranodal marginal zone B-cell lymphoma of MALT type (3 pts.): CD19 + , 
CD20 + , CD22 + , CD79a + , CD23", CD5", CD 10", CD43 +/ " 

Multiple myeloma (diffuse and solitary forms) was diagnosed in 1 8 patients (mean 
age 57.9 years). In six patients (35.3%), the disease developed at the age under 50. 
MM percentage in the patients of Chernobyl clean-up worker group in our study 
turned out to exceed that in the patients of the general populations studied at the 
same period (6.41% vs 4.0%). 



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ECRR Proceedings Lesvos 2009 




Figure 12.13 - BM smears in multiple myeloma: MGG x 900 
Tumors from mature (peripheral) T-cells and NK-cells 

• T-cell prolymphocyte leukaemia (2 pts.): 

CD la", CD2 + , CD3 + , CD5 + , CD7 + , CD4 + ,CD8" 

• Sezary syndrome (3 pts.): 
CD7 + , CD3\ CD4 + , CD8", CD25" 

• Large granular lymphocyte leukaemia 



- T-cell subvariant (3 pts.): CD3 + , CD5 + , CD2 + , CD7 I0W , CD4", CDS , 
CD56 l0W , CD57 +/ , CD16 + , HLA-DR 

- NK-cell subvariant (2 pts.): CD3", CD5", CD2 + , CD7 + , CD4", 
CD8 +/ , CD56 l0W , CD57 + , CD16 + , HLA-DR low 



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ECRR Proceedings Lesvos 2009 




Figure 12.14 - BMfllm of patients with LGL leukaemia (NK-cell subtype): 

a-MGGx900 

b - CD 16 positive cells 

c - CD 5 6 positive cells 



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ECRR Proceedings Lesvos 2009 




Figure 12.15 - Reactive responses in bone marrow stroma in clean-up workers 



Cytochemistry and immunophenotype of stromal dendritic cells: 



Alkaline phosphatase 
Acid phosphatase ++ 

Acid non-specific esterase 
PAS-reaction + 
Vimentin ++ 
HLA-DR + 

DAKO-DRCL - 
CD34 



Reactive responses in bone marrow stroma in clean-up workers with malignant 
diseases of hematopoietic and lymphoid tissue exhibiting the strongly alkaline 
phosphatase-positive villous cells (endothelium of sinuses or blood vessels? cells 
precursors of osteoblasts?). The appearance of these cells in bone marrow of clean- 
up workers (both leukaemia patients and patients with non-malignant diseases of 



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ECRR Proceedings Lesvos 2009 

hematopoietic and lymphoid tissue) could be regarded as a response to incorporation 
of the osteotropic heavy metals including radionuclides in endostal areas. It is highly 
probable that such cells that were not evident in the bone marrow of the patients 
observed in pre-Chernobyl period could serve as the non-specific markers of 
radiogenic leukaemias. This problem deserves further studying. 

All the main forms of malignant diseases of hematopoietic and lymphoid tissues 
including B-cell chronic lymphocytic leukaemia were registered in the group of 
Chernobyl clean-up workers diagnosed in 10-23 years after the exposure to 
radiation. The comparison of the relative distribution of the specified forms of 
hematopoietic and lymphoid malignancies in the patients diagnosed among 
Chernobyl clean-up workers demonstrates the increasing multiple myeloma rate and 
the tendency to the increasing non-Hodgkin's lymphoma in leukaemization phase 
and CML rates as compared to the group of general population. 



35 



30 



# 25 
§ 20 
a> 15 






10 
5 




^ 




53 Clean-up workers 
■ General population 



Multiple myeloma Large granular 
lymphocytic 
leukemia 



Non-Hodgkin's 

lymphoma 

(leukemic 

phase) 



Chronic 

myelogenous 

leukemia 



Figure 12.16 - Relative frequency of selected leukaemia and lymphoma types in 
clean-up workers and general population 



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ECRR Proceedings Lesvos 2009 

The peculiar feature of AML in clean-up workers under study was the development 
of leukaemia on the background of preceding MDS in 19% of all AML cases 
studied. The high incidence of LGL-leukaemia among clean-up workers with 
hematopoietic malignancies (1.77%) is of particular importance since until recently 
this category of T-cell and NK-cell neoplasms was not revealed in 
oncohematological clinics in Ukraine. Only verified precise diagnosis could be the 
prerequisite for the advanced studies in analytical epidemiology of different 
biological types of leukaemias aimed at elucidating the role of the radiogenic factor 
in the pathogenesis of the malignant diseases of hematopoietic and lymphoid tissue. 



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ECRR Proceedings Lesvos 2009 

13 
The ARCH Project and the health effects of the 
Chernobyl accident 



Dr. Keith Baverstock 

University ofKuopio, Finland, ARCH Project 



Agenda for Research on Chernobyl Health 

A European Commission funded project within FP7. 

ARCH will identify and prioritise (short and longer-term) the potential studies, 
examine their feasibility, cost effectiveness and likelihood of success, and 
provide a reasoned and comprehensive strategic agenda for future research. 

Although primarily concerned with the three most affected countries effects 
in wider Europe will also be considered 

You can find out more at the website 

http://arch.iarc.fr 

ARCH needs your input 

ARCH needs to know what you think needs addressing from the RESEARCH 
perspective in relation to the HEALTH EFFECTS potentially arising from the direct 
effects of radiation from the Chernobyl accident (i.e., excluding psychosocial health 
effects). You can make relatively short proposals or comments via the website or 
longer, more comprehensive proposals via e-mail attachment. 

Editors note: October 2011. None of the research proposals suggested by this 
initiative will be funded according to the EC. 



212 



ECRR Proceedings Lesvos 2009 



14 

Radiation induced genetic effects in Europe after the 
Chernobyl nuclear power plant catastrophe 

Prof Hagen Scherb, Dr Kristina Voigt 

Institute of Biomathematics and Biometry, German Research Center for 
Environmental Health, Neuherberg, Germany 

Genetic Effects 

Muller carried out experiments with varied doses of X-rays to Drosophila, and a 
connection between radiation and lethal mutations emerged. By 1928, others had 
replicated his results, expanding them to other model organisms such as wasps and 
maize. A genetic effect, as a definition, may be the result of radioactivity or 
substances that cause damage to (the genes of) a reproductive cell (sperm or egg), or 
a somatic cell, which can then be passed from one generation to another, or may 
induce disease (e.g. cancer) in an individual. Examples can include Sex odds, birth 
defects, stillbirths, leukaemia or thyroid cancer. 

(http://www.doh.wa.gov/Hanford/publications/overview/genetic.html) Muller HJ 
(1927). Artificial transmutation of the gene. Science 66: 84-87 



Genetic theory for the human sex odds at birth 

Irradiated parents and. offspring gender 

Fathers only => sex odds 

Mofheis only -> sex odds 

Both parents -> ??? 

Figure 14.1 - Genetic effects - sex odds (sex ratio) 

Schull WJ, NeelJV (1958). Radiation and the sex ratio in man. Science 128: 343- 
348 



213 



ECRR Proceedings Lesvos 2009 

Dickinson HO et al. (1996). The sex ratio of children in relation to paternal 
preconceptional radiation dose. J Epidemiol Community Health 50(6): 645-652 
Padmanabhan et al. (2004) Heritable anomalies among the inhabitants of regions of 
normal and high background radiation in Kerala. Int J Health Serv 34 (3), 483-515 

Dosimetry 

Working hypothesis 

In the first few years after the ChNPP accident, deposition of 

46.6 kBq/m2 Cs-137 
+ 233 kBq/m2 Cs-134 
generated an effective dose of 1 mSv/a 



Figure 14.2 - Fallout and dose formation 

Jacob P et al. (1990) Calculation of organ doses from environmental gamma rays 
using human phantoms and Monte Carlo Methods. GSF-Bericht 12/90 

Drozdovitch Vet al. (2007) Radiation exposure to the population of Europe 
following the Chernobyl accident. Radiat Prot Dosimetry 123 (4), 515-528 

Bundesamtfur Strahlenschutz (2006). Jahresbericht 2005, p. 36. Editor: Bundesamt 
fur Strahlenschutz, Germany, Salzgitter 

BStMLU and BStMELF (1987). Radioaktive Kontamination der Boden in Bayern. 
Munich: Bayerische Staatsministerien fur Landesentwicklung und Umweltfragen 
(BStMLU) und fur Ernahrung, Landwirtschaft und Forsten (BStMELF) 



214 



ECRR Proceedings Lesvos 2009 



Fig, 1 Stillbirth proportion for the combined two 
most highly contaminated districts in Bavaria: 
Augsburg-aty (53.7 kBq/m ft 2) and Berchtes- 

gaden {50.3 kBq/nV^} including change -point 
(CP) and reduced change- point (CFt) models 



O.DDB 

o.ooe 




♦ 




♦ 








: 007 


* se P 












1 .. 




CPr 




0.0Q6 


► 












O.DD5 - 






V ♦ 








0.004 










♦ ^v 


C 003 












\^ 


: oo2 








-V 






0.001 - 
0000 












"*■ --. ^ 



61 62 6J M «& 89 97 60 60 90 91 92 



Fig. 2 Stillbirth proportions for Bavaria+GDR 
WestBerlin, Denmark, Hungary. Iceland. Latvia, 
Norway, Poland, and Sweden combined, change- 
point (CP) and reduced change- point (CPr) models 




67 66 S9 90 91 92 



Figure 14.3 - Stillbirth in Bavaria, Germany, and stillbirth in Europe, 1981 - 1992 



Ql 



O o r 



o o" 



1977 1982 1987 1992 





Q4 


0.006 I 


O 


0.005 
0.004 


9 o 

° 0o0 ° ;o i 
° ° \: o 




0.003 





1977 1982 1987 1992 



to 



ooo 



Q2 



o o 



1977 1982 1987 1992 



Q5 


9 


4b 

o ° o Q 


. °cP°o° 6 ° | 



1977 1982 1987 1992 







Q3 




0.006 


o°o o 




0.005 
0.004 


\ \ 9 ;\ o 

6 o o°o ° A 
oo 

C 


\ 


0.003 










1977 1982 1987 1992 



Mean uSv 5/86 from Chernobyl 
in Finish Population quintiles 



Ql 
Q2 
Q3 
Q4 
Q5 



13.0 
31.0 
70.0 
137.9 



51.7 



Figure 14.4 - Stillbirth in Finland, 1977 - 1992 (prevalence data by exposure 
quintiles) 



215 



ECRR Proceedings Lesvos 2009 





° * 


0.006 


*S^ o 




<Xn Q ,1 


0.005 


° oB ^^ o 


0.004 


o O^t 


0.003 





1977 1982 1987 1992 




1977 1982 1987 1992 




1977 1982 1987 1992 




1977 1982 1987 1992 




1977 1982 1987 1992 



Mean uSv 5/86 from Chernobyl 


in Finish 


Population quintiles 


Ql 


6.6 


Q2 


13.0 


Q3 


31.0 


Q4 


70.0 


Q5 


137.9 


total 


51.7 



Figure 14.5 - Stillbirth in Finland, 1977 - 1992 (spatial temporal model 



OR per mSr/a 




95% CL 


[1.10, 1.42] 


p-value 


0.0006 



Figure 14.6 - Stillbirth in Finland, 1977 - 1992 (dose specific risk 



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ECRR Proceedings Lesvos 2009 



Bavaria 




Fanner GDR 




4 ta^fc. ..^ 



Cs-137 kBt|/m^2 



ma* = 15-1 



Figure 14. 7 - Sex odds and fallout (dose) in Germany (spatial distribution of fallout) 



(9333 ° 

- "- o 




• 41 

0.00 0.20 0.40 0.60 0.80 1.00 1.20 1.4 

Dose = rnSvte 



OR/tmSr/a) 1-0380 
95%£I [IJ0126.K0640] 

p-vahic 0.0031 



Figure 14.8 - Sex odds and fallout (dose) in Germany (1986+1987 depending on the 
excess dose by Chernobyl fallout: 0.0143 (mSv/a)/(kBq/m2)) 



217 



ECRR Proceedings Lesvos 2009 



1.04 



o 


1.0? 


+-» 




cd 




i- 




</) 




"D 




"D 




O 




X 

o 


1.00 


(/) 





0.98 



Sex odds ratios per mSv/a and 95% CL 
(adjusted for pre period, and non-adj.) 



Q 1.016 



Q 1.005 



' 1.015 



1984/1985 



1986 - 1991 1986 - 1991 (non-adj.) 



Figure 14.9 - Sex odds and fallout (dose) in Germany (1984-1991, long-term dose 
dependent jump heights 1986-1991) 



013 
0009 
0MB 

0.007 
50.006 



■ -■- ■ 


S_uM»r 




lOjpptr 


--D- 


lfr5jflp*r 




ID lower 




199+ 1985 1386 1987 1988 1989 1990 1991 



Hg. S: Birth prevalences of tivo congenital heart malformations 
(ICD745++ttD74tf. 11 = 2797) h Bavaria: stratification according t( 
i of districts [see Table i) 



Figure 14.10 - Congenital malformation of the heart (1984-1991, long-term dose 
dependent jump heights 1987-1991) 



218 



ECRR Proceedings Lesvos 2009 



Similar effects on the sex odds as recently published have already been observed in 
the USA and in Europe on a global scale in the 1960s and 1970s, but have not yet 
been acknowledged as possible effects of atmospheric atomic bomb test fallout. 

Note, the "missing boys" in the "sex ratio literature" may be "less missing girls" 
from the 1970s onward, after the atmospheric atomic bomb test ban. 











516 - 




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• EU 


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615 - 




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1950 i960 1970 1900 1990 MX 






Year 



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Figure 14.11 - Sex odds and atmospheric atomic bomb testing 

M Martuzzi, N Di Tanno, R Bertollini. Declining trends of male proportion at birth 
in Europe. Archives of Environmental Health, 56(4):358 364, Jul- Aug 2001. 

TJ Mathews and BE. Hamilton. Trend analysis of the sex ratio at birth in the united 
states. Nat Vit Stat Rep, 53(20): 1 17, Jun 2005. Nat Cent for Health Stat. 

S Meyer, H Scherb. Untersuchung des jahrlichen Geschlechterverhaltnisses der 
Neugeburten in Europa und den USA auf Changepoints, July 31 2007 (synoptic 
reanalyses). 



219 



ECRR Proceedings Lesvos 2009 



Live birth sex odds: USA 

1.060-1 



i 

s 



1.055- 



1.050- 



1.045- 



1.040 



GL 




— i 1 1 1 1 1 1 1 1 1 r 

1966 1970 1974 1978 1982 1986 1990 1994 1998 2002 2006 2010 



Figure 14.12 - Sex odds in USA, 1970 - 2007 



Europe Ilia, 1970-2007, complete data 



Births and sex odds 



Belgium 

France 

Ireland 



Luxembourg 
Malta 
NGther lands 



Portugal 

Switzerland 

UK 



total 
male 
sex odds 



80,373,314 

41,249,601 

1.0543 



Europe 1 1 lb, 1970-2007, complete data 


Births and sex odds 


Albania 


Germany 


Poland 






Austria 


Greece 


Romania 






Belarus 


Hungary 


Russ. Fed. 






Bulgaria 


Iceland 


San Marino 






Czechoslovakia (f.) 


Italy 


Sweden 






Denmark 


Latvia 


Yugoslavia (f.) 


total 


216,491,268 


Estonia 


Lithuania 




male 


111,258,587 


Finland 


Norway 




sex odds 


1.0573 



Former SU Republics, 1980-2005, incomplete data 



Births and sex odds 



Kazakhstan 
Kyrgyzstan 
Moldova 



Tajikistan 

Turkmenistan 

Ukraine 



Uzbekistan 



total 
male 
sex odds 



47,655,378 

24,463,930 

1.0549 



40 countries with territory in Europe + 4 Asian countries; Spain omitted because of 
unusual trend; also ommitted: Andorra, Liechtenstein, Monaco, Turkey, and Vatican 
due to no data at all, or essentially incomplete data. 

Figure 14.13 - Sex odds in Europe, and parts of Asia, 1970 - 2007 



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ECRR Proceedings Lesvos 2009 



Live birth sex odds: Europe 1 1 1, a 

1.065-1 



CO 

8 

CO 



1.060- 



1.055^ 



1.050- 



1.045- 




ChNPP 

i 1 1 1 1 1 1 1 1 1 1 r 

1966 1970 1974 1978 1982 1986 1990 1994 1998 2002 2006 2010 



Figure 14.14 - Sex odds in Western Europe - less exposed 



Live birth sex odds: Europe 1 1 La 

1.065-1 



co 

i 

CO 



1.060^ 



1.055^ 



1.050- 



1.045 




i 1 1 1 1 1 1 1 1 1 1 r 

1966 1970 1974 1978 1982 1986 1990 1994 1998 2002 2006 2010 



Figure 14.15 - Sex odds in Central and Eastern Europe - moderately or highly 
exposed 



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ECRR Proceedings Lesvos 2009 



Live birth sex odds: Asia 

1.065-1 



— former SU republics 



8 

CO 



1.060- 



1.055^ 



1.050- 



1.045- 




i 1 1 1 1 1 1 1 1 1 1 r 

1966 1970 1974 1978 1982 1986 1990 1994 1998 2002 2006 2010 



Figure 14.16 - Sex odds informer SU republics in Asia - high exposure 

I present a hypothesis - that the jump heights in sex odds after Chernobyl depend 
upon the amount of fallout where the national excess is greater than or equal to 
average effective doses. As you have seen, I have compared the sex odd ratios in 
countries with differing levels of fallout after Chernobyl: low fallout in France, 
intermediate fallout in Denmark, Germany, Italy and the Former Yugoslavia, and 
highest in Belarus and the Russian Federation. 



Live birth sex odds: France 

1.080- 
1.075- 
1.070- 
1.065- 

1.060- 

<D 1.055 
ft 

1.050 
1.045- 



CO 



1.O40 




ChNPP 
1 



1 1 1 1 1 1 1 1 1 1 

1966 1970 1974 1978 1982 1986 1990 1994 1998 2002 2006 2010 



Figure 14.17 - Sex odds in France 



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ECRR Proceedings Lesvos 2009 



Live birth sex odds: Germany 



1.080-r 

1.075- 
1.070- 
1.065- 

1.060^ 
CD 1.055 
1.050H 



tn 



1.045- 



1.040 



o ooo 




i 1 1 1 1 1 1 1 1 1 1 r 

1966 1970 1974 1978 1982 1986 1990 1994 1998 2002 2006 2010 



Figure 14.18 - Sex odds in Germany 



Live birth 


sex odds: Italy 








l.UHU- 
















1,075- 
















1.070- 














(0 

1 

s 

CO 


1.065- 
1.060- 
1.055- 




9 9 


6 


1 o%j5 


\P.!\Q 




6 




1.050- 
















1.045- 
















1040- 






Cht 


^ipp 








19 


1 
66 


i i i i 
1970 1974 1978 1982 


I 1 1 

1986 1990 1994 


i i i r 
1998 2002 2006 20 


10 



Figure 14.19- Sex odds in Italy 



223 



ECRR Proceedings Lesvos 2009 



Live birth 


sex odds: Yugoslavia (f.) 




1.090- 

1085- 

1.080- 

"O 1075- 

1.070- 

CD 1.065- 

CA 

1.060- 

1.055- 

1.050- 
19 




6 ^ 




9 

\QGU \T 

"'"#■■■■■" y 



jpp 


10 


1 
66 


i i i i 
1970 1974 1978 1982 


l l l l l l 
1986 1990 1994 1998 2002 2006 20 



Figure 14.20 - Sex odds in the Former Yugoslavia 



Live birth 


sex odds: Russian Federation 




i.uau- 












1,075- 












1.070- 










CO 
CO 


1.065- 
1.060- 
1055- 
1.050- 
1.045- 




rJ>9® rtj-ca 


<& oP^bp 




t ° 


(^6 eP^psr^ 


/ 




1O40- 




ChNPP 






19 


66 


i i i i i i i i i i r 
1970 1974 1978 1982 1986 1990 1994 1998 2002 2006 2010 



Figure 14.21 - Sex odds in the Russian Federation 



224 



ECRR Proceedings Lesvos 2009 






Live birth sex odds: Belarus 

1.080-r 

1.075- 
1.070- 
1.065- 

1.060^ 
<D 1.055 
1.050 
1.045H 

1.040 



6 







Q l\ Ml 



6 











Q/\p Q0 



6© 



ChN PP 
1 1 1 1 1 1 1 1 1 1 

1966 1970 1974 1978 1982 1986 1990 1994 1998 2002 2006 2010 



Figure 14.21 - Sex odds in Belarus 



Live birth 


sex odds: Denmark 


1.080- 








1.075- 










1.070- 




o 


9 




w 










"O 1.065- 






(9 




1.060- 
ft 




<^-Jite o <■ 




<D 1.055- 

CO 

1.050- 






& 6 b W° 




1.045- 




6 & 


6 




1040- 




ChNPP 




19 


66 


I I I I I I I I I I I 

1970 1974 1978 1982 1986 1990 1994 1998 2002 2006 2010 



Figure 14.22- Sex odds in Denmark 



225 



ECRR Proceedings Lesvos 2009 



Vergleich der in den Jahren 1986, 1987, 1996 und 2006 berechneten effektiven Dosen fur Ervvachsene durch die SSK 



Gebiet 


Effektive Dosis im 1. Jahr (mSv) 


Gesamte effektive Dosis fur die nach 
dem Unfall foJqenden 50 Jahre (mSv) 




1986 


1987 


1996 


2006 


1986 


1987 


1996 


2006 


Voralpengebiet 




1,2 


0,65 


0,5 




3,8 


2,2 


2,1 


Siidlich Donau 


0,5-1,1 


0,6 


0,35 


0,3 


1,5-4,0 


1,9 


1,3 


1,1 


NOrdlich Donau 




0,2 


0,17 


0,1 




0,6 


0,55 


0,4 



Figurel4.23 - Ecological dose-response (German collective dose data) 



Sex odds ratio by "optimum" national average effective dose 
estimates (jump heights in 1987 interpreted as dose) 




0.50 

effective dose [mSv/a] 



Figurel4.24 - Ecological dose-response ("national dosimetry") 



226 



ECRR Proceedings Lesvos 2009 



Country 


jump OR 


mSv/a 


France 


1 .0002 


0.02 


Germany 


1.0018 


0.15 


Italy 


1 .0027 


0.22 


Yugoslavia (f.) 


1 .0074 


0.61 


Russian Federation 


1 .0090 


0.74 


Belarus 


1 .0092 


0.75 


Denmark 


1.0104 


0.85 


jump OR per mSv 


1.0] 


L21 



Figure 14.25 - Optimum excess collective doses per year in France, Italy, former 
Yugoslavia, Russian Federation, Belarus, and Denmark based on the linearity 
assumption, the jump heights in 1987 and the overall excess collective dose in 
Germany of 0.15 mSv/year from 1987 to 2007 (Germany serves as a standard) 



227 



ECRR Proceedings Lesvos 2009 



West Berlin 

0.009i 



C 

o 

t 



Q 



0.006- 



0.003- 



0.000' 





II 
II 

° 



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/i 










D u 



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January 1987 



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o 






itf 



qOOOq ft Q , , e ,_, 

<boo o o omgfc ■■-■ <£ w oo ^ -^b- 



oo |W$o o «i> ^stf 

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6 , o 6 o 



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1983 



1985 



1987 



1989 



1991 



1993 



Belarus 



o.oo3-r 



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t 



Q 



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0.000' 




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6! 



ChNPP 



1981 



1983 



1985 



1987 



— i — 
1989 



1991 



1993 



Figure 14.26 - Down syndrome in Europe before and after Chernobyl (1) 



228 



ECRR Proceedings Lesvos 2009 




Figure 14.27 - Down syndrome in Europe before and after Chernobyl (2) 



Average excess per capita effective dose 
and West Berlin combined 


(mSv) in 


1986 after Chernobyl, 


in 


Bavaria, Belarus 


Region Population 1986 (1000) 


mSv 1986 


Populat 


ion weighted dose 


Bavaria 10,997 
Belarus 10,045 
West Berlin 3,093 




0.47 
0.91 
0.13 






0.21 
0.38 
0.02 


Total 24,135 










0.61 


Doubling dose in mSv 




Estimate 






95%-CL 


Overall excess dose in 1986 

Overall DS odds ratio - 1987 vs. 1986 

Odds ratio per mSv 




0.6 
1.4 
1.7 






1.1 -1.7 
1.2-2.5 


Doubling dose 




1.3 






0.8 - 4.0 



Figure 14.28 - Down syndrome in Europe before and after Chernobyl (3) 



229 



ECRR Proceedings Lesvos 2009 

I have submitted these and their related findings under the title "Low dose ionizing 
radiation increases the rate of nondisjunction in man", with the kind assistance of 
Sperling K. {Institute of Human Genetics, Charite - Universitaetsmedizin Berlin, 
Germany), Neitzel H. {Belarus Institute for Hereditary Diseases, Minsk, Republic of 
Belarus) and Zatsepin I. {Institute of Biomathematics and Biometry, Helmholtz 
Zentrum Miinchen -German Research Center for Environmental Health, 
Neuherberg, Germany). 



Possible scale of lost or impaired children after Chernobyl in all of Europe 
and the part of Asia covered 



Expected 



1937 is Births 5 2007 

male 

female 

sex odds 

missing boys 

missing girls 



Births 
male 
female 
sex odds 
sex OR 



sex OR/mSv 
1.0145(1.0021-1.0271) 



1987^Births^2D07 

BD 3%(LB)+0.5%(TB) 

OR/mSv* 

BD doubling doae 

OR BD+SB 

Excess BD+SB 



Lost or impaired children 



183 802 030 

94 446 693 

89 355137 

1.0570 

249554 

831846 



184 683 430 

94 696 447 

90186 983 

1.0500 

1.0066 (1.0052-1.0070) 



0.400 



183 802 030 

6 437 680 

1.54 

1.61 

1 22 

1 415 709 



2.5 millions 



Live birth sea odds: Europe t p.o, Asia (Oetrenoed) 





r^GK^O 


o 0xft&? 


■ ■.1... 


&/. 




T^eo — . — . — , j\ **r — . — , — . — . — . — 



«e tfra tst4 



r «! -3* XM V&* **» 2Q02 »» XX 




Figure 14.29 - Possible scale of reproductive detriment due to the Chernobyl 
accident (Scherb H, Weigelt E. (2003) 

Conclusions 

UNSCEAR {UNSCEAR 2001 Report, Hereditary Effects of Radiation, Scientific 
Annex, p. 82) states "The estimate of risk" (at 1 Gray) "for congenital abnormalities 
is about 2,000 cases per million live births (compared to 60,000 cases per million 
live births)". 

RR/lGy=62,000/60,000=1.033 

This means: 

Doubling Dose=21. 3 Gy 

As we have shown for congenital malformations {Scherb H, Weigelt E. Congenital 
Malformation and Stillbirth in Germany and Europe Before and After the Chernobyl 
Nuclear Power Plant Accident. ESPR - Environ Sci & Pollut Res, 10 Special (1) 



230 



ECRR Proceedings Lesvos 2009 

2003 Dec, 117-125) {Sperling K et al. Low dose irradiation and nondisjunction: 
Lessons from Chernobyl, 19th Annual Meeting of the German Society of Human 
Genetics, April 8-10, 2008, Hanover, Germany, Abstractbook, p. 174-175) e.g. 
malformations of the heart, deformities, Down syndrome, using data from the 
Bavarian congenital malformation data set, the doubling dose is in the order of 
magnitude of below a few mSv. Thus, UNSCEAR is in error at least at 3 orders of 
magnitude. 

The consistency of our results implies that either there is harm of ionizing radiation 
below 1 mSv, or the dose concept is invalid altogether, or that the exposure after 
Chernobyl was higher than assumed, or even some combination of these concepts. 
The genetic effects of ionizing radiation in humans, animals (and plants) 
should be investigated more objectively and more thoroughly, focusing on birth 
defects, stillbirths, secondary sex ratio, cancer induction, e.g. leukaemia, 
combinatory effects (radiation & chemicals) and synergistic effects. 

"In our own view, it is quite possible that a permanent doubling of the 
"background" dose of ionizing radiation, worldwide, would very gradually 
double mankinds burden of inherited afflictions — from mental handicaps to 
predispositions to emotional disorders, cardio-vascular diseases, cancers, 
immune-system disorders, and so forth. Such a doubling would be the greatest 
imaginable crime against humanity (nature ...)" 

Figurel4.30 - A Wake-Up Call for Everyone Who Dislikes Cancer and Inherited 
Afflictions (Spring 1997) By John W. Gofman, M.D., Ph.D. Egan O'Connor, 
Executive Director of CNR 

Further publications 

I have produced a number of publications on the subject of fallout and its genetic 
effects for futher reading, they can be found below. 

Perinatal mortality and stillbirths 

Scherb H, Weigelt E, Bruske-Hohlfeld I European stillbirth proportions before and 
after the Chernobyl accident. Int J Epidemiol. 1999 Oct;28(5) 
Scherb H, Weigelt E, Bruske-Hohlfeld I Regression analysis of time trends in 
perinatal mortality in Germany 1980-1993. Environ Health Perspect. 2000 
Feb; 108(2) 

Birth defects 

Scherb H, Weigelt E Congenital Malformation and Stillbirth in Germany and Europe 
before and After the Chernobyl Nuclear Power Plant Accident. ESPR - Environ Sci 
& Pollut Res, 10 Special (1) 2003 Dec, 1 17-125 



231 



ECRR Proceedings Lesvos 2009 

Scherb H, Weigelt E Cleft lip and cleft palate birth rate in Bavaria before and after 
the Chernobyl nuclear power plant accident [Article in German, Abstract in 
English]. Mund Kiefer Gesichtschir. 2004 Mar;8(2): 106-10 
Sperling K, Neitzel H, Scherb H (2008) Low dose irradiation and nondisjunction: 
Lessons from Chernobyl, 19th Annual Meeting of the German Society of Human 
Genetics, April 8-10, 2008, Hanover, Germany, Abstractbook, p. 174-175 



Sex odds in Europe 

Scherb H, Voigt K Trends in the human sex odds at birth in Europe and the 
Chernobyl Nuclear Power Plant accident. Reproductive Toxicology, Volume 23, 
Issue 4, June 2007, Pages 593-599 

Scherb H, Voigt K Analytical ecological epidemiology: Exposure-response relations 
in spatially stratified time series. Environmetrics, published Online: 12 Sep 2008 

Relevant demographic databases 

http://data.euro.who.int/hfadb/ 

http://data.un.org/Data.aspx?d=POP&f=tableCode%3a4 

http://data.un.org/Data.aspx?d=POP&f=tableCode%3A54 

http://unstats.un. org/unsd/demographic/products/dyb/dyb2 .htm 

http://www.coe.int/t/e/social_cohesion/population/BELTAB2.xls 

http://epp.eurostat.ec.europa.eu/portal/page?_pageid=0,1136184,0_45572595&_dad 

=portal&_schema=PORTAL 

http://www.johnstonsarchive.net/policy/abortion/ab-poland.html 



232 



ECRR Proceedings Lesvos 2009 



15 



In Utero exposure to Chernobyl accident radiation and the 
health risk assessment 



Prof. Angelina Nyagu 

President, International Physicians of Chernobyl, Kiev Ukraine 

We must first ask a question: what do we know about the qualitative and 
quantitative effects of ionizing radiation on the developing embryo? 




fl 3.10 ?0 0.30 Q.SC 100 

FffttlAJHcrtHlDow.Gv 



Figure 15.1 - Specific radiation effects on foetus: mental retardation, microcephaly 
- Japanese study 

The study shown in Figure 1 shows that those exposed at a gestational age of 8-15 

weeks were most at risk. Survivors of the atomic bombing in Japan who were 

exposed in utero during this sensitive period show a linear increase in the frequency 

of mental retardation with radiation dose (40% per Gy). There were 2,800 people in 

this study. 

However, there is evidence that radiation affects intelligence (Figs 2-3). John 

Gofman writes: 

"In-utero irradiation during the vulnerable period causes the brilliant to become less 

brilliant, the average to become "below average," and the retarded to become more 

retarded. And by pushing more people over the heavy vertical line into the realms of 

mental retardation and sever retardation, such exposure automatically increases the 



233 



ECRR Proceedings Lesvos 2009 

percent of a population-sample which is retarded and severely retarded. (John 
Goffman, 1994)" 



■ Average 


New Percent/ 


Percent Increase in Rate 


FetatDase OldPercentof 


Mental Retardation 


■ 4rads 


(2.63/ 2.28) -1.15 


15 % Increase 


10 rads 


(3.13/ 2.28) = 1.37 


37% increase (at the 

optimum "hermetic" dose) 


- 15.4 rads 


(3.77/2.28)= 1.65 


65% increase 


- 23.0 rads 


(4.75/ 2.28) -2.08 


2.08-fold increase 


- 30.8 rads 


(6.00/ 2.28) -2.63 


2*£3-fold increase 


• 46.2 rads 


(9.12/ 2.28) = 4.00 


4-fold increase 


■ 61.5 rads 


(13.36/2.28) = 5.8* 


5.S4kfold increase 


■ 72.0rads 


(16.85/2.28)-7.39 


7.39-fold Increase 



Figure 15.2 - Tabulations of CNR (John Gofman criticism) 







1 1 










~\ 












F%we -A 


Bti^bcned vet = 
2,23 ft cf total. 










fi] 


" 


























t ;i 


" 






















Li 




























- "- 




























« I 


" 


























Ml 





























I 

I 

■3 







\ 1 






\ 




~i 












Figure -B 


Blackened arc* s 


1 1 














\ 














1 -il 












\ 












fci 










i 
















; - "i 










J 




\ 












3 ' 










I 




\ 












i m 








J 


1 






\ 


<. 


fc~n 









McflUJ Fuittlim in Stanford Score Unjta, 
Hmv-j 1 verticAl line - cruot of Rtafditian. 



Mwitil Fwwti™ ib Sludon) Scot? Units. 
Heavy vertical Line ■ tmet of * 



Figure 15.3 - How Many People Are Mentally Retarded? (Gofman) 

There are widely established effects that radiation has on the embryo: these include 
intrauterine growth retardation (IUGR), embryonic, foetal, or neonatal death, 
congenital malformations and cancer. 



234 



ECRR Proceedings Lesvos 2009 



Gestational 


Stage 


Radiogenic effects 


0-9 days 

Embryo 
contains only 
few cells 
which are 
not 
specialized. 


Preimplantation 

Before about 2 weeks gestation the 
health effect of concern from an 
exposure of > 0.1 (Gy) or 10 rads is 
the death of the embryo. Because the 
embryo is made up of only a few 
cells, damage to one cell, the 
progenitor of many other cells, can 
cause the death of the embryo, and 
the blastocyst will fail to implant in 
the uterus. Embryos that survive, 
however, will exhibit few congenital 
abnormalities. 


If too many cells are damaged - 
embryo is resorbed. 

If only few killed - remaining 
pluripotent cells replace the cells 
loss within few cell divisions; 

Atomic Bomb survivors - high 
incidence of both - normal birth 
and spontaneous abortion. 

For all stages, one has to expect 
induction of childhood cancers, 
in particular, childhood 
leukaemia's. The risk of 
childhood leukaemia's can be 
shown to be increased down to 
doses of 10 mGy. The doubling 
dose is in the range of 30 mGy. 
One must keep in mind, 
however, that the spontaneous 
risk is small: about 5 per 
1 00. 000 children per year. Thus, 
a very small risk is doubled by 
about 30 mGy. 


10 days-6 
weeks 


Organogenesis 

Radiation risks are most significant 
during organogenesis and in the early 
foetal period somewhat less in the 
2nd trimester and least in the third 
trimester 


Most risk 

Congenital anomalies, growth 
retardation, 

mental retardation 


6 weeks- 
40 weeks 


foetal 


Growth retardation, 
microcephly, mental 

retardation 



Figure 15.4 - Embryonic risks at each stage of gestation 



235 



ECRR Proceedings Lesvos 2009 



Phenomen 


Patholog 


Site 


Diseases 


Risk 


Definition 


on 


y 










Stochastic 


Damage 


DNA 


Cancer 


Some risk 


Incidence of 




to a single 




germ cell 


exists at all 


the disease 




cell may 




mutation 


doses; at 


increases but 




result in 






low doses, 


the severity 




disease 






risk is 
usually less 
than the 
spontaneou 
s risk 


and nature of 
the disease 
increase with 
dose 


Threshold 


Multiple 


Multiple 


Birth 


No 


Both the 




cell and 


variable 


defects, 


increased 


severity and 




tissue 


etiology, 


growth 


risk below 


incidence of 




injury 


affecting 


retardation, 


the 


the disease 






many 


death, 


threshold 


increase with 






cellular 


toxity, 


dose 


dose 






and 


mental 










organ 


retardation 










functions 


etc. 







Figure 15.5 - Stochastic threshold dose-response relationships of diseases 
produced by environmental agents (Brendt, 1987,1990,1999) 



LMMnC^-flQOnd) 



BHkcdM *TIQ (251*30 pita*); 
Scree nam ntwbtlM n 41% *f ra 



Enfr A/9ta 15niiki 





Figure 15. 6 - Foetal Effects of Ionizing Radiation: Severe Mental Retardation 



236 



ECRR Proceedings Lesvos 2009 

Sources: ACOG Committee on Obstetric Practice. ACOG Committee Opinion. 
Number 299, September 2004 (replaces No. 158, September 199 5). Guidelines for 
diagnostic imaging during pregnancy. Obstet Gynecol 2004 Sep; 104(3): 647-51; De 
Santis M, Di Gianantonio E, Straface G, et al. Ionizing radiation in pregnancy and 
teratogenesis: a review of literature. Reprod Toxicol 2005 Sep-Oct;20(3): 323-9; 
Harding LK, Thomson WH. Radiation and pregnancy. Q J Nucl Med 2000 
Dec;44(4):317-24; Henshaw SK. Unintended pregnancy in the United States. 
FamPlann Perspect 1998 Jan-Feb; 30(1): 24-9, 46; International Atomic Energy 
Agency. Radiologic protection of patients: pregnancy and radiationin diagnostic 
radiology, [online], [cited 2008 Jan 21]. Available from Internet: 
http://rpop.iaea.org/RPoP/RPoP/Content/SpecialGroups/l_PregnantWomen/Pregn 
ancyAndRadiology.htm; International Commission on Radiological Protection. 
Radiation and your patient: a guide formedical practitioners. Ann IRCP 
2001;31(4):5-31; International Commission on Radiological Protection (ICRP). 
Biological effects after prenatal rradiation (embryo and foetus). ICRP Publication 
No. 90. Kidlington, Oxford (United Kingdom) : Elsevier; 2003; International 
Commission on 

Radiological Protection (ICRP). Pregnancy and medical radiation. ICRP 
Publication No. 84. Kidlington, Oxford (United Kingdom) : Elsevier; 2000;Timins 
JK Radiation during pregnancy. N J Med 2001 Jun;98(6):29-33; Toppenberg KS, 
Hill DA, Miller DP. Safety of radiographic imaging duringpregnancy. Am Fam 
Physician [online]. 1999 Apr 1 [cited 2008 Jan 21]. Available from Internet: 
http : //www. aafp.org/afp/99040 1 ap/ 1 8 1 3 .html 



237 



ECRR Proceedings Lesvos 2009 



Spontaneous incidence of major malformations 


Approximately 


l%to3% 




Intrauterine growth restriction 


4% 


Spontaneous abortion 


At least 15% 


Genetic disease 


8% to 10% 


Mental retardation (intelligence quotient less than 70) 


Approximately 


3% 




Severe mental retardation (unable to care for self) 


0.5% 


Heritable effects 


l%to6% 


Spontaneous risk of childhood leukemia and cancer (ages to 15) 


0.16% 


Children developing cancer up to age 15 (United Kingdom) 


0.15% 


Children developing leukemia only to age 15 (United Kingdom) 


0.03% 


Lifetime risk of contracting fatal cancer 


20% 


Lifetime risk of contracting cancer 


33% 



Figure 15. 7 - Background Incidence of Conceptus Complications without 
Diagnostic Imaging Radiation 

Source; ACOG Committee on Obstetric Practice. ACOG Committee Opinion. 
Number 299, September 2004 (replaces No. 158, Septembel995)Guidelines for 
diagnostic imaging during pregnancy. Obstet Gynecol 2004 Sep; 1 04(3) : 647-5 1 ; 
Brent RL. The effects of embryonic and foetal exposure to x-ray, microwaves, and 
ultrasoundln: Brent RL, Beckman DA, editors. Clinics of perinatology, teratology. 
Vol 13. Philadelphia (PA): Saunders; 1986:61 3-48; Coakley F, Gould R. Guidelines 
for the use of CT and MRI during pregnancy and lactation. Chapter 5. In: UCSF 
imaging of retained surgical objects in the abdomen and pelvis section handbook 
[online]. University of California, San Francisco Department of Radiology. 2005 
[cited 2007 Jun 6J. Available from Internet: 

http://www.radiology.ucsf.edu/instruction/abdominal/ab_handbook/05- 
CT _MRI_preg.html; Harding LK, Thomson WH. Radiation and pregnancy. QJNucl 
Med 2000 Dec;44(4):317-24; International Commission on Radiological Protection. 



238 



ECRR Proceedings Lesvos 2009 

Radiation and your patient: a guide for medical practitioners. Ann IRCP 
2001 ;3 1(4): 5-31; International Commission on Radiological Protection(ICRP). 
Biological effects after prenatal irradiation (embryo and foetus). ICRP Publication 
No. 90. Kidlington, Oxford (United Kingdom) : Elsevier; 2003 international 
Commission on Radiological Protection (ICRP). Pregnancy and medical radiation. 
ICRP Publication No. 84. Kidlington, Oxford (United Kingdom) : Elsevier; 2000; 
Ratnapalan S, Bona N, Chandra K, et al. Physician 's perceptions of teratogenic risk 
associated with radiography and CT during early pregnancy. AJR Am J Roentgenol 
2004 May; 182(5): 1107-9; Ratnapalan S, Bona N, Koren G. Ionizing radiation 
during pregnancy. Can Fam Physician 2003 Jul;49:873-4; Sharp C, Shrimpton JA, 
Bury RF. Diagnostic medical exposures: advice on exposure to ionizing radiation 
during pregnancy [online] . Chilton, Didcot, Oxon (UK): National Radiological 
Protection Board. 1998 [cited 2007 Jul 19]. 

Available from Internet: http://www.e 

radiography.net/regsetc/nrpb_asp8/Diagnostic Medical Exposures Advice on 
Exposure to Ionising Radiation during Pregnancy.htm; Timins JK. Radiation during 
pregnancy. N J Med 2001 Jun;98(6):29-33; Toppenberg KS, Hill DA, Miller DP. 
Safety of radiographic imaging duringpregnancy. Am Fam Physician [online]. 1999 
Apr 1 [cited 2008 Jan 21]. Available from Internet: 
http://www.aafp.ors/afp/990401ap/1813.html . 

Threshold dose for developmental effects approximately 0.1 Gy. 

At 0.1 Gy , increase of 0.1-1%. ICRP (1990 Recommendations of the International 
Commission on Radiological Protection. Report 60.) recommends a limit of 
radiation exposure to a member of the general public as 100 mrem/y (1 mSv/y) and 
the limit for the foetus of an occupationally exposed individual to 200 mrem (2 
mSv) during the gestation period. There was a long-standing debate on whether a 
threshold dose exists for the weeks 8 to 15, whereas it was comparatively clear from 
the beginning that a threshold dose is present for weeks 16 to 25. Biology always 
pointed to threshold doses for both time periods, because many cells have to be 
killed or impaired in their migration behaviour in order to cause a severe mental 
retardation. ICRP meanwhile suggests a threshold dose of about 300 mGy for both 
time intervals. It is not clear whether a threshold dose exists for IQ reduction. This 
question will be hard to answer in any case, because even if one assumes linear dose 
dependence without a threshold, the risk in the low dose range will be so low that it 
is impossible to detect it. ICRP estimates the risk to be a reduction of 21 IQ-points 
per Gray for the weeks 8 to 15, and 13 IQ-points per Gray for weeks 16 to 25. Both 
numbers do not include the cases of severe mental retardation. Chernobyl 
caused significantly lower external foetal doses, but it caused the high doses on the 



239 



ECRR Proceedings Lesvos 2009 

foetal thyroid by the incorporation of the radioiodine and other radionuclides in first 
stage of accident. 

A Ukrainian investigation 

A recent investigation in the Ukraine showed promise. The objectives of the study 
was the psychometric, neurophysiological and neuropsychiatric (ICD-10) criteria) 
characterization of acutely prenatally irradiated children. This study involves acutely 
prenatally exposed children — born between April 26th, 1986 and February 26th 
1987 from pregnant women at the time of the accident who had been evacuated from 
the 30-kilometer zone surrounding the Chernobyl NPP to Kiev — and their 
classmates. This sample seems to be optimal for examination of possible 
distinguished effects of exposure in different periods of cerebrogenesis. During the 
first stage (1990-1992) it was examined children five-six years old. At the second 
stage (1994-1996) the epidemiological WHO project "Brain Damage in Utero" 
(IPHECA) was implemented. At the third stage (2002-2004) it was examined a 
cohort of 154 children born between April 26th 1986 and February 26th 1987 to 
mothers who had been evacuated from Chernobyl exclusion zone to Kiev and 143 
classmates from Kiev. In the third stage reconstruction of individual doses of 
children born to mothers evacuated from the Chernobyl exclusion zone was carried 
out at taking internal and external exposure. Children were profoundly medically 
examined by general paediatrist, paediatrist-psychoneurologist, paediatrist- 
endocrinologist, paediatrist-Ear-Nose-Throat (ENT), paediatrist-ophtalmologist, 
paediatristcardiologist, paediatrist-haematologists, paediatrist-pulmonologists, 
paediatrist-gastroenterologists, paediatrist-surgeon, paediatrist-gynecologist (for 
girls), general and biochemical blood tests, immunological tests, urine tests, 
coprogram, thyroid and visceral ultrasonography, Electrocardiogram (ECG), 
electroencephalogram (EEG), rheoencephalogram (RhEG) as well as 
fibrogastoscopy, cardiac ultrasonography, and magnetoresonance imaging (MRI) 
for diagnostic reasons. It should be emphasised that neuropsychiatric assessments 
presented here are based on neurological and psychiatric examinations, psychometry 
of both children and their mothers. 

In order to avoid uncertainties concerning the estimation of prenatal age at the time 
of the Chernobyl accident we used the formulas offered for estimation of prenatal 
age at atomic bombing in Hiroshima and Nagasaki: Days of pregnancy (Y) = 280 — 
(date of birth — April 26th, 1986), where the day of birth has been obtained by 
interviewing the mothers of the children. The mean duration of pregnancy is taken to 
be 280 days. The days from birth were counted back until the accident and 
subtracted from the 280 days, the duration of a pregnancy. Since the duration is 
calculated from the beginning of the last menstrual cycle, additionally 14 days have 



240 



ECRR Proceedings Lesvos 2009 

to be subtracted. Gestational weeks after fertilization at the time of the accident were 
thus calculated by the following equation: Gestational weeks (G) = (Y — 14 days) / 
7 days, where G was taken to be zero if GO. According to different radiosensitivity 
of the foetus the gestational time is divided into 4 periods in relation to the 
Chernobyl accident. In the exposed groups there are fewer children who were at the 
earliest stages of prenatal development. A possible explanation is increased numbers 
of abortions and miscarriages due to the Chernobyl accident. 

Individual reconstruction of total foetal doses, foetal thyroid doses and foetal doses 
on the brain has been carried out using 2 methods: 

1) foetal thyroid dose is assumed to be equal to the thyroid dose of the mother, and 

2) according to the model by ICRP Publication 88 (2001). 

The main irradiation sources of the pregnant women were: 1) external irradiation of 
the whole body; 2) irradiation of thyroid by radioactive iodine isotopes; 3) internal 
irradiation by inhaled radionuclides; 4) internal irradiation by ingestion of 
radioactively contaminated food. The doses were reconstructed for the exposed 
children from Pripyat and also for the control group in Kiev by Professor Victor 
REPIN (Laboratory of dosimetry RCRM in Ukraine). 

First stage 



s 




Acutely exposed group 
Comparison group 



20 



40 



60 



80 



100 

Ptoses mSv 



Distribution of foetal dose of external irradiation 

Acutely exposed group (M±SD) 31. 7 ±14.4 rrrSv 

Comparison group — 1.9±8.1 mSv 

Figure 15.8 - Dose on embryo and foetus distribution (ICRP-88) 



241 



ECRR Proceedings Lesvos 2009 

There are 20 children from Pripyat (132%) who had been exposed in utero >100 
mSv - the threshold for medical abortion due to prenatal irradiation (European 
Commission, 1998; ICRP Publication 84, 2000). 



# 



100 
80 
60 
40 
20 




■ Acutely exposed group - 
d Compa rison group _ 



it 



10 20 30 40 50 60 



70 

Dose,mSv 



Distribution of equivalent doses on the foetal brain 

Acutely exposed group (M ±SD) 20 .5±9.4 mSv 

Comparison group — 0.7±1.5 mSv 

Figure 15.9 - Dose on embryo and foetus distribution (ICRP-88) 



242 



ECRR Proceedings Lesvos 2009 



D 



30-km Zona 



■ Cctfifcmin&fedr 
territories 



i Control 



100 




0,01-0,35 0,36-0/75 0,76-1,0 



Figure 15.10 - In UTERO Thyroid doses were estimated 0,01 - 3,34 Gy. 

The mean doses according trimester of gestation: 

Until 8 weeks -0,0 Gy; 

of 8 to 15week-0,31Gy; 

ofl6to25week-0,8Gy; 

More than 25 weeks - 0, 62 Gy. 



243 



ECRR Proceedings Lesvos 2009 



% 



100 

90 
SO 
70 
60 
50 
40 
30 
20 
10 




■M 



□ Exposed group In Prlpyat 

(ii=1S2) 
■ Comparison group from Kiev 

(n=143) 



Ihnrft 



,ni i 



5 i 5 



= g i 5 a 

Dose raige,mSr 



5 i S i i *. 



a 



Exposed group (M±SD) — 760.4±631.8 n^Medim — 7463 mSv 
Comparison group — 44.5±43.3 mSvj Me dim — 274 mSv 



% 



100 
90 
SO 
70 
60 
50 
40 
30 
20 
10 




:M 



□ Exposed group In Prlpyat 

(n=152) 
■ Comparison group from Kiev 

(n=143) 



Itadtni 



ni i 



"' 5 * * 



HHHH1S5 

is i i I i *. 



5 2 5 5 S 
Dose raige,mSr 



a 



Exposed group (M±SD) — 760. 4*631.8 n^Medim — 7463 mSv 
Comparison group — 44.5±43.3 m$Y s Me dim — 274 mSv 



Figure 15.11 - Dose on thyroid in utero distribution (ICRP-88): There are (35.5%) 
children from Pripyat who received in utero thyroid doses >1 Sv 



244 



ECRR Proceedings Lesvos 2009 




0-7 



8-15 



16-25 



26+ 



Weeks of gestation 

Figure 15.12 - Geometric means of the thyroid doses in utero related to the periods 
of cerebrogenesis at 26.04.1986 in exposed group in Pripyat 

According to the model by ICRP-88 there is a strong influence of gestational age on 
the thyroid doses in utero: later intrauterine period at the time of exposure — higher 
the thyroid doses in utero. It is concluded that multifactor impact of Chernobyl 
disaster unfavourable factors defined health deterioration in children irradiated in 
prenatal period shortening amount of practically healthy kids down to 5%. The 
results showed much more somatic diseases and neurovegetative mental disorders. 
At the same time it was clearly recognized the decrease of immunity (hypo 
immunoglobulin level and increase of T-lymphocytes, T-helpers), neurological, 
gastrointestinal and endocrine diseases. 



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ECRR Proceedings Lesvos 2009 



Health groups 

Average doses of gamma-irradiation 
varied as 7mSv-13 mSv (Monte- 
Carlo dose reconstruction method for 
foetus).Individual dose of Thyroid - 
varied within 10-120cSv. 


Main group (n=147) 

(Evac. From 30-km 
Zone) 


Control group 
(n=101-city. Kiev) 


a 


b(%) 


a 


b(%) 


1-st -healthy children 


12 


8,2 


2 


2 


2-nd -dynamic diseases 


68 


46,3 


67 


67 


3-rd -chronic relapsing diseases 


55 


37,4 


30 


30 


4-th - chronic decompensate diseases, 
congenital defects, anomalies 


7 


4,8 


2 


2 



Figure 15.13 - First Stage (children 5-6 years old) 



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ECRR Proceedings Lesvos 2009 



lTl'^lTlol tnl 




0,8 1 

Thyroid foetal dose, Gv 



Figure 15.14 - Thyroid-stimulating hormone (TSH) 

It was also established in this cohort that starting with the 0.3 Gy threshold dose 
thyroid-stimulating hormone (TSH) level grew along with foetal thyroid dose 
increase. Thereupon the radiation-induced malfunction of the thyroid-pituitary 
system on this stage was suggested as important biological mechanism in the genesis 
of health risk assessment and mental disorders of prenatally irradiated children. 






felllM 






' 1 



""■"■■■ ESS 






D'S'© * 



~~ 



mm 



:r\-- -M 1 ...fc-IM 



- A- 



■ ' J. ... Jji AlT U. 



Or 

.- 



esI;5 DE^SEl' 



^::: ■■■{ : -;:::^ 



1 S::= 



1 



h».£2j. «***.,* 



» llft#... K_ 19, »- feUprW* « - KpmTW 



Figure 15.15 - 

(1) Distribution of the psychic development level disturbances in children 
irradiated in utero during the pregnancy 1-3 trimesters: a- the norm; b- below 
the norm ; c- psychic development delay. 

(2) The levels of separate psychic functions development ( 6 years old): 1- notions; 



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ECRR Proceedings Lesvos 2009 

2-psychomotor system; 3 -attention; 4-memorizing. a ,b - 1 trimester, b,c - 3 
trimester (control and irradiated children accordingly). The Kern-Jeracika and 
verbal tests of willingness to teaching (school education) were used. 

Signs of mental progress retardation were met in 77% of kids from Pripyat city 
exposed in utero within first pregnancy trimester, in 69% of those exposed in 
second trimester and in 45% — in third one. Among kids resident in Kiev city the 
percent of persons with decreased mental development value was substantially lower 
(p<0.05). In 25.5% of cases in Pripyat group the brain organic pathology signs were 
revealed. Brain circulation disorders according to the rheoencephalography data 
were observed a bit more often in children from Pripyat city exposed to radiation 
within first pregnancy trimester. The low induces of psychic development in utero 
irradiated children are largely determined by the irradiation factor. 

Second Stage: WHO project "Brain Damage in Utero" (IPHECA) 

An analysis of the results in three countries (Belarus, Russian and Ukraine) has 
shown the following: An incidence of mild mental retardation in prenatally 
irradiated children is higher when compared with the control group; an upward trend 
was detected in cases of behavioral disorders and in changes in the emotional 
problems in children exposed in utero; incidence of borderline nervous and 
psychological disorders in the parents of prenatally irradiated children is higher than 
that of controls. In the frame of the WHO Pilot Project «Brain Damage in Utero» we 
have previously revealed a significant increase of borderline and low range IQ, 
emotional and behavioural disorders. Since possible dose correlations were not 
investigated and contradictory results of the mental health assessment of the in utero 
exposed children and the aetiology of the observed neuropsychiatric disorders were 
found. 



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ECRR Proceedings Lesvos 2009 



Groups 


Number of children with revealed mental retardation 
IQ<70. 

A decrease in high (IQ>110), as well as statistically 
significant higher prevalence of mental retardation 
(IQ<70) in Ukrainian prenatally irradiated children 
compared to the controls: 21 (3.9%) vs. 12 (1.6%) 
correspondingly (^2=6.27; df=l; P<.05). 


Number of kids with emotional, 
behavioural and non- 
differentiated disorders 


Indices characterising 
degree of mental 
health in mothers 


Methods 


Non- 
verbal 
intellect 

(Draw- 

a-Man) 


Verbal 

intellect 

(BPVS) 


Non-verbal 
intellect 

(Raven 
Coloured 

Matrices) 


General 
intellect 
lowering 
(A)* 


General 

intellect 

lowering 

(B)** 


Ratter 

scale 

A(2) 


Ratter 

scale 

A(2) 


General 
Health 
Question- 
naire 

GHQ-28 


IQ 


«Experimental» 

n=544 


11 

(2.06 
%) 

n=535 


61 

(11.34%) 

n=538 


59 

(10.95 %) 
n=539 


19 

(3.49 %) 
n=544 


23 

(4.34%) 

n=544 


152 

(41.76%) 

n=364 


137 

(34.86%) 

n=393 


24.26±0,4 
n=382 


33.6± 
0,6 

n=377 


PFor c2 or 

Student's 

criteria 


>0.05 


>0.05 


>0.05 


<0.05 


<0.05 


<0.01 


>0.05 


<0.01 


<0.05 



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ECRR Proceedings Lesvos 2009 



Control, 


8 


66 


92 


8 


16 


214 


269 


20.73±0,5 


43. 6± 


N=759 


(1.06 


(8.87 %) 


(12.12%) 


(1.05%) 


(2.10%) 


(28.69 %) 


(38.93 %) 


n=639 


0,5 n=750 




%) 


n=744 


n=759 


n=759 


n=759 


n=746 


n=691 








n=755 



















Figure 15.16 - Mental health in children exposed to radiation in prenatal period and their mothers 



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ECRR Proceedings Lesvos 2009 



T*M 







Non-verbal intelligence («Drsw-e- 
Man» test) 



[Q itat! 



110 L10J* >m 




Verbal intelligence 

(^British Picture Vocabulary Scale*) 



=30 ft.9! 91-110 1U0-UD >1« 

Non-verbal intelligence (« Raven Coloured Matrices ») 



Figure 15.17 - Distribution oflQ scores in the prenatally irradiated children 
(((Experimental)) group) and non-exposed control children 



251 



ECRR Proceedings Lesvos 2009 



FW-rt 









F&-A J[ .I^W^/ V^W^ 
tiTTi ■ J..-.. . - .^-. "J ^ t - ■ j i ii : 



Pl-fl 



TlUlgrnptiy 




Figure 15.18 - Conventional EEG ofB-v 23. 12.1998. Without anticonvulsants. The 
3rd minute of hyperventilation — paroxysmal activity (like «spike-waves») in the 
fronto-temporal area shifted to the left (leads F7,T3, T4, T5, T6J.-MRI 
(1998&1999). 



252 



ECRR Proceedings Lesvos 2009 



E EG- [j mi. i. em 



Children 
exposed lu 
radial tun in 

IJUfimiiil periud 
n=50 



Sfl«J%) 



23f46JK) 



U(UJK) 



HHOJ%> 



30AJK) 



LlftfJK) 



T(14Jtt) 



Children from 

I '/Jlll'Lll "l'UUf J 

n=50 



24(4*0 *») 



■ (UuOK) 



2(4JK> 



f(12AH) 



U0Mtt) 



10(2M%) 



32(*U%) 



activity pottsiB In 
to then 




La»-rotteg*EEG (23-23 ft?) 




tfdov (ty andJatfflQefbfytagriurmA 



hi the 



qfnormai 



Figure 15.19 - Bioelectrical patterns in prenatally irradiated children 

Abnormal EEG patterns in irradiated children displayed themselves in a number of 
ways. Low-voltage EEG (20-25 (iV) with excess of slow (§) and fast ((3) activity 
together with depression of a- and 0-activity with paroxysmal activity shifted to the 
left fronto-temporal region was one of the most distinguished conventional EEG- 
pattern in the children of the acutely exposed group (31% vs. 8%, %2 = 16.85, 
P<.001). Disorganised slow EEG-pattern with 5-activity domination characterised 
by disorganised activity of moderate (40-55 (iV) or high (70-80 (iV) amplitude 
with a mainly 5-range slow activity domination and non-regular a-activity where 
hyperventilation led to bilateral paroxysmal activity discharges, as well as 
disorganised EEG-pattern with paroxysmal activity, similar in general to the one 
described above, but characterised by generalised paroxysmal discharges and bursts 
of acute, 0- and 5-waves of high amplitude where the hyperventilation led to the 
bilateral paroxysmal activity increase, were found equally in the both groups. 
Finally, an epileptiformal EEG with «spike» or «polyspike — wave» complexes in 
the fronto-temporal region, mainly of the left hemisphere, and bilateral paroxysmal 
activity in the form of 5-waves of very high amplitude (higher than 100 (iV) was 



253 



ECRR Proceedings Lesvos 2009 



another of the most distinguished conventional EEG-pattern among the children of 
the acutely exposed groups. 



NON-RADIATION 
FACTORS 



RADIATION 
FACTORS 



Mother low education. 
level 



Delivery 
compH cations 



Mental health 
worsening in mother 



h=0.8 


VERBAL IQ 
DECREASE 




h=0.8 


h=0.3 


MOM- VERBAL IQ 
DECREASE 






h=0.5 


EMOTIONAL- 
BEHAVIOURAL 
DISORDERS 



h=0.3 



Residence territory UT Cs - 
contamination, level in prenatal 
period 



b=0.4 



Cerebrogenesis most critical period 

(8—15 weeks of prenatal progress) at 

the time of Chernobyl disaster 

(0426.1986) 



h=0.6 



Internal radiation dose 
on thyroid 



Figure 15.20 - Factors making impact on mental health in children exposed to 
radiation in prenatal period 

Third Stage 

A number of assessments were carried out here, these included: 

• Intellige 
nee Assessment by the adapted and normalised version for the Ukrainian 
children of the Wechsler Intelligence Scale for Children, WISC (the verbal, 
performance and full scale IQs). 

• Addition 
al Psychological and Demographic Measurements 

• Russian 
translation of Achenbach's Child Behaviour Checklist (CBCL) 

• Rutter A 
(2) Behaviour Rating Scale 

• General 
Health Questionnaire (GHQ-28) 



254 



ECRR Proceedings Lesvos 2009 



The 
vocabulary subtest of the Wechsler Adult Intelligence Scales (WAIS) 

Impact 
of Events Scale (IES) and Irritability, Depression Anxiety Scale (IDA) 

Self- 
rating Depression Scale (Zung's) 

Question 
naire on stress-factors related to the Chernobyl accident 

School 
performance 

Demogr 
aphic background, family history, educational level of the family, social and 
economical status as well as they completed a standardised questionnaire on 
radiation history 



Clinical Psychiatric and Neurological assessment according to ICD-10 




■ Acutely exposed 
group 

D Comparison group 



0-7 8-15 16-25 26+ Weeks after fertilisation 

Distribution of children by prenatal age at the time 
of explosion (April 26th, 1986) 

Figure 15.21 - As titled 



255 



ECRR Proceedings Lesvos 2009 

In the exposed group there are fewer children who were at the earliest stages of 
prenatal development (0-7 weeks after conception) that could be explained with 
abortions and miscarriages due to the Chernobyl accident. 



90 
80 
70 

60 
50 
40 
30 
20 
10 




# 





n 


1 




P < .001 




LL 










p < .001 




- ■ Acutely exposed group 
~ d Comparison group 














. ■ 




■ 





1st 



2nd 



3rd 



4th 



5th 



Health group 
Distribution of children by the health groups 

1st — absolutely healthy; 2nd — prac tic a l^ healthy; 3rd — remission of 

chronic diseases; 4th — handcapped chicken with chronic dseases; 5th — 

hnixhcapped cnkven with decompensated dseases 



Figure 15.22 - Health groups 



256 



ECRR Proceedings Lesvos 2009 




* 60 










50 

40 


-■Acutely exposed group 
_c Comparison group 




<ttl 


1 






VI - 






■3U 

» 

to 




<JU 




■ 






. ^1 


■ 



Comparison 
mPripyat gFeupfro&t Aiev 



• Lower full scale IQ 



m 71-M B1-10D 101-120 U1-M0 140-> 

Distribution of full scale IQ 

Tktr* oro *ig$nfh*Kf {P*&QQ1) 



Figure 15.23 - Wechsler Intelligence Scale for Children (WISC): Full scale IQ 




nr Fripjat grwtpjrms Xrcr 
ftt=146) (ft=136) 



of 
tk 

more simple with low IQ ami less 
j high IQ in exposed group. 



Figure 15.24 - Intelligence of children (WISC): Verbal IQ 



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ECRR Proceedings Lesvos 2009 



MOf" 




iooJ^ 



50 i 


. 






W 












35 


= 


1 Acutely exposed group 
D Comparison group 




m 










Ht 








is 


■ 




£U ■ 
15 
10- 
5 

0- 


an. ■ 




1 






1 


<JB 







Lxpo&dgroap Camparam 
in Ftipymi gnmpjnm Mtier 
(n-146) fa-I34) 



<7Q 71-H Bl-lll 111-121 121-140 l«-> 

Ann 

Difbibutiim of perfbrm^noe IQ 

Differences on 
performance IQ are 
nonsignificant (P>0*05) 



Figure 15.25 - Intelligence of children (WISC: Performance IQ) 



ior" 



There at* significant 
(P<8.d01) differences on 
intelligence of exposed 
children: 




in Pwipyat 
fH-14$} fn-136} 

Higher IQ discrepancies due 
to verbal IQ deterioration 



WISC 



p*-«K«--a p* > *»* ■« ■»■» p^^+»» 



ilQ-wMIty 



Figure 15.26 - Intelligence of children (WISC) .'Discrepancies IQp-IQv 



258 



ECRR Proceedings Lesvos 2009 



IQ distribution, control children 



1.0 

o.s 

0.2 
0.7 
0,6 

0.5 
0.4 
D.3 

0.2 
1 
0.G 



vlQ 
pIQ 



1 



40 60 SO 100 120 140 160 

IQ 



Verbal IQ 




100 120 140 160 

IQ 



* EL 



IQ distribution, exposed 

t^liildr on 



1 
0;9 

0.0 
0.7 
C6 
OS 
O r 4 
Q : 3 
: 2 
0.1 



pra 

v id 






j/ 



# 



100 12G 

IQ 



140 1S0 



Performance IQ 



1 
0.9 

0.8 
0.7 
0.6 
0.5 
0,4 
0.3 
0.2 
0.1 




Exposed children 
Control children 



J 



I 



f 



W~ 



...* ' / 



40 GO 80 100 120 140 100 

IQ 



Figure 15.27 - Fraction of control and exposed children below specific verbal and 
performance IQ, 



FETAL DOSE = -8,345 + 1 ,998 * IQPJGV 
Correlation: r = 0.53; p<0.018 



130 



110 



ST 90 

60 

E 



70 



uj 50 



30 



10 



*l^******C.* i..*..--..i..~. .".."..! 

^^+f^ * i -* ' " I 

• * ; 



24 28 32 36 40 44 48 52 

IQ discrepancy "performance IQ - verbal IQ" 



56 



Regression 
95% confid. 



Figure 15.28 - Correlation between IQ discrepancy ((performance IQ - verbal IQ» 
and foetal dose in children irradiated in utero, who have IQ discrepancy > 25 point 



259 



ECRR Proceedings Lesvos 2009 



140 

130 

120 

110 

100 

90 

SO 

70 

60 

50 



0.0 



20 



16 



12 



0.0 



Foetal thyroid dose vs. Verbal IQ 
Verbal IQ= 1 14.07 - 1 5.64 * Foetal thyroid dose 
Correlation: r = -.3S95; p = .023 



■o _ --a ° 


^~~^--^^;-- --^.. ... 


o '":~-o.^ ^~~~t~—-—__ 
; ; ; l...?.:.-.^.. 



0.4 0.6 1.2 

Foetal thyroid dose, Gy 



1.6 



"tk Regression 
2.0 95% con fid. 



Foetal thyroid dose vs. Vocabulary subtest of WISC 

Voca bu la ry = 1 5. 1 03 - 5. 1 30 * Fo eta I thyroid dose 

Correlation: r = -.5075; p = .002 



- --C?!^ 


o 

CD 

O 
O 
O 

O 


















■ 


~ ■- ■. 


-_- 


o 


-- 


o 




---- 


^-—-__o 


o 




o 
















o 






"■■-■. 



0.4 



O.fi 1.2 

Foetal thyroid dose. Gy 



1.6 



2.0 



Nx, Regression 
95%confid. 



Figure 15.29 - Relationships between Verbal IQ and Vocabulary subtest of WISC vs 
foetal thyroid dose, in children of the both groups (n=47) exposed at 16-25 weeks 
after fertilisation 



260 



ECRR Proceedings Lesvos 2009 



V1Q = 1 13.4 - 004 * Dose on myroW in utero 
Correlation: r = -0.16 (P=0.D09) 



% : o 

Eft ■ ^ 

x^ ^w ir *^ ^ioa^--o- ---a.;-- . 

g ^ n " ^""^--^tr -- — *— L__ 

>p ° oo °o b ]""^--i. 

^ fcoi o ° ° ; '"— • 

boo o 

$ o° 

o 

b 



140 

130 

il20 

"110 



ioo -H 

90 
80 
70 



<M 



<;oi 



0.044.3 131-C.S 0.61-10 

"a. Regression . 




c Full Scale :q 

■Verbal B] 

_ LPerfomarcelQ 



"hyro'd fo?fe dose, Cy 



500 1OO0 1500 2000 2500 30W) 3500 
floss on Ihyod in i terr (mSv) 



Children iirtelloenoe in proportion to thethyroid tocbl dose 



Figure 15.30 - Correlations between verbal IQ of children of both groups and dose 
on thyroid in utero (ICRP-88) 




Expand group Camparuax 
UtPripvat group frost EUf 
(k-70) (k-77) 

• Somatization 



■ Acutely exposed group 
Q Comparison group 



Emotional and behavioural sphere of 
exposed chBdren sfgnfficaittfy 
p*&9*} mo»e afflers with: 



Figure 15.31- Behavioral and emotional problems. Children. Achenbach test (Youth 
Self Report). Somatic complaints (T) 



261 



ECRR Proceedings Lesvos 2009 




67+* 



Expaaeignap Coaeparisoa 
te Ifripyet gtonpjrout Kle 
(n=7W (n=77) 




Mhquuit Mwbur and rntomlUng 



Children of the exposed group show an increased level of emotional and 
behavioural problems In comparison with chUdrenfrom Kiev (P<8L 95) 

Figure 15 32 - Achenbach test (Youth Self-Report): Total score (T) 




Exposed group Comparison 
m Pripyat group from Kiev 
(n=7&) (rt=77) 































<034 



























Acutely expend pnziup 

Total behavioral aid enotional pnblciiB 
accord n0 to Adnnbadt test 



Children of the exposed group 
shew an increased level of 
emotional and behavioural 
problems in comparison with 
children from Kiev (P<#.&5) 



Figure 15.33 - Achenbach test (Youth Self-Report): Total score (T) 



262 



ECRR Proceedings Lesvos 2009 



Epilepsy 

Migraine 

Headache syndromes 

Sleep disorders 











<.O01 


1 ' 1 




1 1 


^^H 


■ Acutely exposed group 
D Comparison group 


^mml <.05 










I 1 


1 <.05 





20 40 60 ^ 80 

Diseases of the Nervous System (ICD-10) 



Figure 15.34- As titled 



Organic asthenic dlsoides 

Organic personalty disorder 

Somatoform autonomous dysfunction 

Nsurasthenb 

MmnnjnilrAkAp riknnbtK 

Mental retardation 

Disorders of psychological development 







™, 1 1 1 1 1 1 1 




"" " ' « 




1 1 1 


< 


L 
01 


















l«.o: 






















^^ 
















<,W3 




■ Acutely exposed group 
D Comparison group 


1 




1 1 








.001 










<.0S 








- 










■J < 






























— 1 — 1 — 1 — 





3 



13 20 23 30 33 40 43 



Mental and Behavioural Disorders (ICD-10) 



Figure 15.35 - As titled 



263 



ECRR Proceedings Lesvos 2009 



US 




Mothers of children evacuated from Pripyat 

experienced much more (P<0.001) 

real stress events 

(evacuation, lade of 

information about relatives, migration, 

difficulties of medical care, etc) 

There is a significant (PO.WH) mental health 

problems in mothers of children evacuated from 

Pripyat: PTSD (0,001) 

Depression (0,001) 

Somatoform disorders (0,001) 

anxiety, insomnia (0,001) 

Social dysfunction (0,04) 

Severe depression(0,01) 



Figure 15.36 - Mother 's stress events 

The results of this study agree with the Japanese studies concerning the critical 
periods of cerebrogenesis — 8-15 and, especially, 16-25 week after fertilisation, the 
dose related full scale IQ reduction and the increase of paroxysmal disorders. 
The highest vulnerability of the brain under exposure at 16-25, but not 8-15 weeks 
after fertilisation as in the Japanese sample, we can explain this through maximal 
radioiodine transfer rate in foetal thyroid at about 20-25 weeks and more «delicate» 
examination of intelligence disturbances that corresponds exactly to the events of 
the brain creation at 16-25 weeks after fertilisation (apoptosis and its underlying 
molecular mechanisms; growth factor gene expression, cell formation and 
migration; neuronal differentiation, gross anatomical parameters in cortical and 
commissural diameters, synaptogenesis and synaptic remodelling limbic system 
and brain asymmetry forming, etc.). An absence of dramatic increase of mental 
retardation, especially its severe form, as well as microcephalia obviously can be 
explained by significantly lower foetal doses of irradiation than that in the atomic 
bomb survivors and lack of information about all in utero survivors. It is need the 
strong epidemiological investigation of the whole of this cohort. The «dose — 
effects» relationships concerning both intelligence and EEG-parameters, which are 
the most marked at the critical periods of cerebrogenesis, testify to significant 
contribution of prenatal irradiation into the brain damage. 

Thus, the neuromental health of the acutely prenatally irradiated children at the 
Chernobyl exclusion zone is deteriorated in comparison with the non-evacuee 
classmates living in Kiev due to more frequency of episodic and paroxysmal 



264 



ECRR Proceedings Lesvos 2009 

disorders, organic, including symptomatic, mental disorders, somatoform autonomic 
dysfunction, disorders of psychological development, and behavioural and 
emotional disorders with onset usually occurring in childhood and adolescence. 
Obviously, their neuromental health disorders are etiologically heterogeneous 
including psycho-social and economic factors, medical problems in their families; 
however an effect of real stress events (but not only their perception) during 
pregnancy together with prenatal irradiation cannot be excluded. Intelligence of the 
acutely prenatally irradiated children is deteriorated due to reduction of full scale 
and verbal IQ, as well as WISC performance/verbal discrepancies, with verbal 
decrements. In spite of the children's intelligence is multifactorial, the contribution 
of prenatal irradiation was revealed. Characteristic neurophysiological changes of 
the acutely prenatally irradiated children are also etiologically heterogeneous, but 
the dose — effect relationship, especially at critical periods of cerebrogenesis, can 
testify the impact of prenatal irradiation. This study suggests that prenatal exposure 
to ionising radiation at thyroid foetal dose 0.2-2 Gy and foetal dose 1 1-92 mSv can 
result in detectable brain damage. The data obtained reflect great importance, 
interdisciplinarity, and complexity of such problem as brain damage in utero 
following radio ecological disaster and a necessity to integrate international efforts 
to its solving. Thus this integrate research conducted in this area has made a 
valuable contribution to radiological protection by reinforcing the view that 
functionally significant radiation effects on the developing brain are most likely to 
occur at the low doses. 

Finally, the TSH level grows with foetal thyroid dose increase with a 0.3 Sv 
threshold. Probably, these children had been affected by intrauterine hypothyroidism 
resulted in intelligence disturbances during the life. Obviously, an international 
psychoendocrine study should be organise for exploration of functions of the 
pituitary-thyroid system as a possible biological basis of mental health problem in 
children irradiated in utero as a result of the Chernobyl disaster. Neurophysiological 
abnormalities together with intelligence disturbances, both dose-related, especially 
at 16-25 weeks after fertilisation, as well as a «concentration» of the most severe 
neuropsychiatric disorders among the children exposed at the critical periods of 
cerebrogenesis, can testify to the developing brain abnormalities due to multiple 
factors with effects of prenatal irradiation. Consideration must to given to 
deterministic effects prevail during the initial phase of damage may subsequently be 
modified by compensation within the brain. 

In this view this study should be continued. We must study the whole of this cohort 
of children irradiated in utero in Ukraine, identify further children irradiated in 
utero and children exposed at the age of 0-1 years is necessary; identify and form 



265 



ECRR Proceedings Lesvos 2009 

cohorts of age-, gender- and urban/rural-matched children from radioactively clean 
areas of the Ukraine; verify and develop the currently available dosimetric models; 
assess and verify the multifarious neuropsychiatric disorders; carry out a risk 
analysis of the influence of radioiodine in prenatal period and during the 1st year of 
life on brain development and a risk assessment of other stochastic and non- 
stochastic diseases on this base. A large-scale epidemiological investigation on 
this cohort only will give us the answer on open question on low dose risk after 
in utero radiation. It seems that the acutely prenatally exposed children at the 
Chernobyl exclusion zone are a unique sample that should be used for the 
reassessment of the risks of prenatal irradiation at radiation accidents on nuclear 
reactors. 



266 



ECRR Proceedings Lesvos 2009 

16 

The real effects of the Chernobyl accident and their 
political implications 

Alexey V. Yablokov 

Russian Academy of Sciences, Moscow 



I start by calling to attention our publication in Volume #1171 of the Annals of the 
New York Academy of Sciences, which will be published in English (enlarged and 
revised) in the book "Chernobyl: Consequences of the Catastrophe for People and 
Nature" by A. Yablokov, M. Nesterenko and A.Nesterenko (St. Petersburg, "Nauka" 
Publ.,2007, 372 p.) Hundreds of individuals and organizations help us made this 
mega-review. This is very likely the broadest scope and undoubtedly the most up-to- 
date monograph about the Chernobyl consequences. 

Among reasons complicating an estimation of the impact of the Catastrophe 
on health, singular is the Official secrecy and falsification of the USSR medical 
statistics for the first VA years after the Catastrophe. These created difficulties in 
estimating true individual doses in view of a reconstruction of doses in the first days, 
weeks, and months; uncertainty as to the influence of "hot particles"; problems 
accounting for spotty contamination and an inability to determine the influence of 
each of many radionuclides, singly and in combination. The demand by IAEA and 
WHO experts to require "significant correlation" between the imprecisely calculated 
levels of individual radiation (and thus groups of individuals) and precisely 
diagnosed illnesses as the only iron-clad proof to associate illness with Chernobyl 
radiation is not scientifically valid. 

Objective information on the impact of the Catastrophe on health can be 
obtained comparing: morbidity / mortality of territories having identical 
physiographic, social, and economic backgrounds and differ only in radioactive 
contamination; the health of the same group of individuals during specific periods 
after the Catastrophe; the health of the same individual in regard to disorders 
specifically linked to radiation (e.g., stable chromosomal aberrations); health of 
individuals living in contaminated territories by the level of incorporated 
radionuclides; and by correlating pathological changes in particular organs by 
measuring their levels of incorporated radionuclides. 



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ECRR Proceedings Lesvos 2009 



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•Bryansk oblast 
■Kaluga oblast 



t 1 — i — r 



1 r 



<& <£> o> o& <&> <xS <# <& <£ qN &, <£> qIx <#> <$ cA $ $ 

Figure 16.1 -All solid cancers in Bryansk and Kaluga provinces and Russia (Ivanov 
et al, 2004) 

Among specific disorders associated with Chernobyl radiation, there is increased 
morbidity and prevalence in the blood and the circulatory system; endocrine system; 
immune system ("Chernobyl aids," increased incidence and seriousness of all 
illnesses); respiratory system; urogenital tract and reproductive disorders; 
musculoskeletal system (including composition of bones: osteopenia and 
osteoporosis); central nervous system (changes in frontal, temporal, and 
occipitoparietal lobes of the brain, leading to diminished intelligence and 
behavioural and mental disorders);eyes (cataracts, vitreous destruction, refraction 
anomalies);digestive tract; congenital malformations and anomalies (including 
previously rare multiple defects of limbs and head); thyroid cancer (Chernobyl 
thyroid cancers rapid and aggressive, striking children and adults); leukaemia (not 
only in children and liquidators, but adult population) and other malignant 
neoplasms. Amongst other health consequences of the Catastrophe, exist Intensified 
infectious and parasitic diseases (e.g., viral hepatitis and respiratory viruses), 
premature aging in both adults and children, multiple somatic and genetic mutations 
and most common within these is polymorbidity (people are often afflicted by many 
illnesses at the same time). 

Chernobyl has "enriched" medicine with terms and syndromes never seen before: 
"Cancer rejuvenescence," 



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ECRR Proceedings Lesvos 2009 

"Vegetovascular dystonia", 
"Incorporated long-life radionuclides", 
"Acute inhalation lesions of the upper respiratory tract". 
"Chronic fatigue syndrome," 
"Lingering radiating illness syndrome", 
"Early aging syndrome". 
"Radiation in utero," 
"Chernobyl AIDS," "Chernobyl heart," "Chernobyl limbs," etc. 

But most importantly the full picture of the deteriorating health of those in the 
contaminated territories is still far from complete. Medical, biological, and 
radiological research must expand and be supported to provide the full picture of 
Chernobyl's consequences. Instead this research has been cut back in Russia, 
Ukraine, and Belarus. Psychological factors ("radiation phobia") simply cannot be 
the defining reason because morbidity continued to increase after the Catastrophe, 
whereas radiation concerns have decreased. What is the level of radiation phobia 
among voles, swallows, frogs, and pine trees, which demonstrate similar health 
disorders, including increased mutation rates? 

The Chernobyl Forum (2005) declared that the total death toll from the 
Catastrophe would be about 9000 and the number of sick about 200,000. Soon after 
the catastrophe the average life expectancy decreased noticeably and morbidity and 
mortality increased in infants and the elderly in the Soviet Union. Analyses of 
official demographic statistics in the contaminated territories of Belarus, Ukraine, 
and European Russia, give the Chernobyl death toll here for the first 15 years after 
the Catastrophe amounted to nearly 237,000 people. It is safe to assume that the total 
Chernobyl death toll for the period from 1987 to 2004 has reached nearly 417,000 in 
other parts of Europe, Asia, and Africa, and nearly 170,000 in North America, 
accounting for nearly 824,000 deaths worldwide. 



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ECRR Proceedings Lesvos 2009 



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contaminated by the Catastrophe provinces with the six less contaminated 
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270 



ECRR Proceedings Lesvos 2009 



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Switzerland and Sweden, 1980 - 2006, and undisturbed trend line. Based on official 
statistical data (Korblein, in litt., 2008) 



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ECRR Proceedings Lesvos 2009 

All affected populations of plants and animals (that have been the subjects of 
detailed studies) exhibit of morphological deformities that were rare prior to the 
Catastrophe. In the contaminated territories all plants, fishes, amphibians, birds, and 
mammals that were studied presented lower stability of individual development 
(determined by level of fluctuating symmetry). The number of the genetically 
anomalous and underdeveloped pollen grains and spores in the Chernobyl 
radioactively contaminated soils indicates geobotanical disturbance. All the plants, 
animals, and microorganisms (that were studied in the Chernobyl territories) have 
higher levels of mutations than those in less contaminated areas. 

The chronic low-dose exposure in Chernobyl territories results in a trans- 
generational accumulation of genomic instability, manifested in cellular and 
systemic effects. Wildlife in the heavily contaminated Chernobyl zone sometimes 
appears to flourish, but the appearance is deceptive. According to morphogenetic, 
cytogenetic, and immunological tests, all of the populations of plants, fishes, 
amphibians, and mammals that were studied there are in poor condition. This zone is 
analogous to a "black hole" — some species may only persist there via immigration 
from uncontaminated areas. The tragedy of Chernobyl showed that societies 
everywhere (especially in Japan, France, India, China, the United States, and 
Germany) have to have of independent radiation monitoring of both food and 
individual irradiation levels Monitoring of incorporated radionuclides, especially in 
children, is necessary around every NPP. This monitoring must be independent of 
the nuclear industry and the data results must be made available to the public. The 
WHO diminished the impression of the catastrophe's consequences because it is 
tightly tied to IAEA by agreement, allowing the nuclear industry to hide from the 
public any information that they want kept secret. 

Article III - Exchange of information and documents [ 

1 . The International Atomic Energy Agency (IAEA) and the World Health 
Organization (WHO) recognize that they might have to take certain 
restrictive measures to ensure the confidentiality of information that were 
provided to them . 
Figure 16.6 - Agreement WHO-IAEfrom May 28, 1959 (Resolution WHA 12-40) 

The Chernobyl catastrophe demonstrates that the nuclear industry's willingness to 
risk our planet with nuclear power plants will result, not only theoretically but 
practically, in the same level of hazard to humanity and the Earth as nuclear 
weapons. What happened to voles and frogs in the Chernobyl zone shows what can 
happen to humans in coming generations: increasing mutation rates, increasing 
morbidity and mortality, reduced life expectancy, decreased intensity of 
reproduction, and changes in male/female sex ratios. 



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ECRR Proceedings Lesvos 2009 

17 
Sex ratio of offspring of A-bomb survivors - 
Evidence of Radiation- induced X-linked lethal mutations 

VT Padmanabhan 
vtpadma@yahoo.com 

Abstract. 

According to genetic theory, females exposed to ionizing radiation before 
conception will have lower proportion of boys in their offspring. Likewise, males' 
exposure will result in fewer girls. In 1953, Neel and Schull reported changes in sex 
ratio (SR- males per 1000 females) in the children born during 1948-53 (Phase I) to 
parents exposed to radiation from the atom bombs in Hiroshima and Nagasaki. As 
the findings were in line with the theory, the study was extended for another eleven 
years (Phase II). According to the latest paper published in 1981, the findings in the 
second phase contradicted those of the first phase and hence the observed deviations 
were dismissed as accidental and biologically insignificant. A closer look at two 
papers of the same study published in 1965 and 1981 reveals that 1819 boys and 753 
girls were added to the Phase II database in the 1981 report without any explanation. 
SR of all children born during 1954-65 was 1071 in 1965 report and 1100 in 1981 
report. Even though there were changes in data for the period 1948-53, these were 
minimal and the effect on SR was marginal. There were two control groups in this 
study and SR of these groups during Phase I were 1034 and 1089. SR of all children 
born in Japan during 1950-55 was 1055. Reanalysis of data using the Japanese SR as 
the reference shows that (a) SR of all children in the study was 1075, significantly 
different from the reference (Chi square 6.36, p=0.0117) (b) SR of one of the 
'unexposed' control groups was 1089, significantly different from the national SR 
(Chi square 8.54, p=0.0034), (c) the other 'control' group had a lower SR of 1034 
and (d) all the nine cohorts in the reanalysis had deviant SR, four of them pro- 
theory. The deviances in (b) and (c) above could have been due to the inclusion of 
fathers and mothers exposed to residual radiation from neutron activation products 
and fission products respectively. Incidentally, these two groups were treated as 
control groups in all the genetic studies conducted in the target cities. All genetic 
studies done in Hiroshima-Nagasaki need be reviewed. 



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ECRR Proceedings Lesvos 2009 



Introduction 

In 1927, Herman J Muller observed that female fruit flies (Drosophila Melanogaster) 
exposed to ionizing radiation (IR) had more female progenies [1]. This was the first 
experimental demonstration that IR can induce genetic mutation. Further 
experiments showed that there were more males among the offspring of exposed 
males. The deficit of boys and girls have been attributed to lethal mutations on the X 
chromosome in ova and sperms respectively. A dominant lethal mutation of the X 
chromosome in the sperm will be lethal for the female zygotes as only the daughters 
inherit the paternal X chromosome. The same mutation on the ovum will be lethal 
for both male and female zygotes. A recessive lethal mutation on X chromosome of 
the ovum will be lethal to male progeny only, since the male has only one copy of 
that chromosome. A female receiving an X chromosome with a recessive lethal 
mutation may grow up and reproduce, but all her male zygotes receiving the mutated 
chromosome will be unviable. Therefore, the genetic expectation is that lethal 
mutation on X chromosome of the sperm and the egg will cause a deficit of girls and 
boys respectively in the Fl generation (Fig 1). As the exposure of the population to 
IR was increasing since World War II, an expert committee of the World Health 
Organization (WHO) in 1957 recommended a study of the sex ratio (SR - number of 
boys per 1000 girls) of children of those exposed as this endpoint can be studied 
with limited resources [2]. 

EFFECTS ON IMMEDIATE POST-EXPOSURE (TWO YEARS) 

EXCLUDED 

THE X-LINKED LETHALITY 

• DOMINANT LETHAL MUTATION IN SPERM LETHAL FOR 
FEMALE ZYGOTES ONLY 

• RECESSIVE LETHAL MUTATION IN OVA LETHAL FOR MALE 
ZYGOTES ONLY 

• ALL OTHER LETHAL MUTATIONS GENDER NEUTRAL 

Fig 17.1. Genetic effects of ionizing radiation 

Few studies of children born to radiation workers [3], down- winders [4] and 
residents of high natural background radiation regions [5] have demonstrated a 
significant increase in the incidence of chromosomal and genetic disorders. These 
findings are not accepted by the radiation standard setting agencies because there 



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ECRR Proceedings Lesvos 2009 

was no significant increase in any of the genetic endpoints among the children born 
to the Hibakushas in the bombed cities of Hiroshima and Nagasaki. 

Study of Genetic Effects in Children of the Bombed Cities 

The Atomic Bomb Casualty Commission (ABCC) was constituted in 1945 to 
conduct short and long term human health studies of the bombs in the target cities. 
ABCC was disbanded in 1975 and its structures and functions were transferred to 
the Radiation Effects Research Foundation (RERF), a private foundation funded by 
the governments of the USA and Japan. The first attempt (GE-3 study) to assess the 
radiation-induced genetic effects was initiated by ABCC in 1948. This focused on 
five pregnancy outcomes- still birth, congenital anomalies, birth-weight, perinatal 
mortality and sex ratio at birth (Fig 2). 



METHODOLOGY -GE- 3 STUDY 

• WOMEN 20 WEEK GESTATION, INTERVIEWED WHILE 
REGISTERING FOR RATIONS 

• MIDWIFE VISITS AFTER TERMINATION 

• ALL "NOT NORMAL" AND A THIRD OF THE NORMAL 
CHILDREN SEEN BY A DOCTOR 

• 

LIMITATIONS OF GE-3 STUDY 

• EXCLUSION OF THE RICH 

• ABORTION < 20 WEEKS NOT DETECTED 



Fig 17.2 GE3 Study protocols 

Analysis of data of 75,000 children born during 1948-53 showed a statistically 
significant decrease in SR of children born to the exposed women (p <0.05%) and 
an insignificant increase in SR of children sired by the exposed men [6]. Since this 
finding was pro-genetic theory, ABCC launched the second phase of SR study, 
based on births between 1954 and 1965. In the latest report of the study published in 
1981, the authors concluded that the results of Phase II were opposite to that of 
phase I and the earlier finding was fortuitous and of no significance [7] (Fig 3-6) 
We will take a closer look at the data and the analysis and see if there were any real 
changes in SR that can be attributed to radiation-induced mutation. 



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ECRR Proceedings Lesvos 2009 



"THE FINDINGS OF PHASE II (1954-62) OPPOSITE IN DIRECTION OF 

1948-53 

THE CHANGES OBSERVED IN PHASE I FORTUTIOUS AND 
BIOLOGICALLY INSIGNIFICANT." 

"SEX-LINKED DOMINANT MUTATION MAY NOT KILL FEMALE 
ZYGOTES BECAUSE OF LYONIZATION (INACTIVATION OF THE 
SECOND X CHROMOSOME)" 

Fig 17.3 Sex ratio 1948-53 in two reports, 1966 and 1981 



■ 1965 RffORT ■ 1981 RffORT 



1100 



1080 



1060 



1040 



1020 



1000 





NIC- NIC Father Exp Mother Exp Both Exp Total 



Fig 17.4 Sex ratio 1948-53 (Phase I) for different groups in the RERF studies in 
1965 and 1981. 



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ECRR Proceedings Lesvos 2009 



■ 1965 RH 3 ORT 


m 1981 RH^ORT 


1200 






1150 


■ 


■ 


1100 




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1000 


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NIO NIC Father 


Mother Both Bcp Total 


B<p 


Bcp 



Fig 17.5 Sex ratio 1954-62 (Phase II) in the RERF studies in 1965 and 1981 



BOYSADDBD ■ GIRUSADDBD GIRUSRBVIOVBD 



2000 



1500 



1000 



500 




I 




NIC- NIC Father Exp M other Both Exp Total 
Exp 



Fig 17.6 Boys and girls added to the 1954-62 birth group 

Radiations from the bombs - Gamma Rays, Fission Products and Neutron 
Activation Products 

A short narration of the physics of the bombs will be essential for reviewing the 
health studies in the bombed cities. The explosive yields of the uranium235 (U235) 
bomb dropped in Hiroshima on 6th Aug 1945 was 15,000 tons (15 kilotons - KT) of 
trinitrotoluene (TNT) equivalent. The yield of the plutonium239 (Pu239) bomb 
used in Nagasaki on 9th August was 21 KT [8]. One ton of yield is generated from 
fission of about 1.45x1020 atoms. Fission of one atom generates about one free 
neutron that does not take part in the chain-reaction, two fission products (FP) and 
200 MeV of energy in the forms of photon, heat and blast. The free neutron will 



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ECRR Proceedings Lesvos 2009 

enter the nucleus of the atom it encounters and transform it into neutron activation 
product (NAP). Neutrons, FP and NAP are radioactive. FP yield was 4.35x1024 in 
Hiroshima and 6.09x1024 in Nagasaki. Less than 10% of the fissile materials in a 
bomb will undergo fission, the remaining fuel and other materials will evaporate in 
the inferno. The bomb debris and materials consumed in the fire will be lofted into 
the air and drifted by wind and return to the ground as fallout in due course. 
People were exposed to the gamma rays, neutrons, particles of unfissioned uranium 
and plutonium, FP and NAP. The exposure to gamma rays was external and 
instantaneous and was confined to a circle of about 3000 meters radius from the 
hypocenters. FP and NAP also delivered internal doses through air, water and food 
on a chronic basis till all of them decayed to their stable isotopes. NAP intensity 
was the highest near the ground zeros while the fallout was dispersed in a wider 
area. Koi-Takasu (off Hiroshima) and Nishiyama (off Nagasaki), which are about 3 
km away from the hypocenters, got drenched in the fall-out, which was referred to 
by the local people as black rain. NAP and FP were sources of chronic internal and 
external radiations for those who worked and lived around the hypocenters and the 
fall-out areas. The radioactivity recorded on 1st November 1945 was four times the 
background level at Koi Takasu, eight times at the Hiroshima hypocenter and ten 
times at Nishiyama. Arakawa estimated the maximum exposure to a resident at 
Nishiyama at 10-rad [9] (Fig 7,8). He took into account only the external exposure; 
the internal doses from inhaling the radioactive dust and eating foods harvested from 
the contaminated soil and waters were not included in the estimate. 





■ M ale Nishiyama ■ M ale Control 






Female Nishiyamaa Female Control 




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30 


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(pCi/kg body weight); Internal body burden higher 24 yrs after bomb 



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ECRR Proceedings Lesvos 2009 



1 
0.8 
0.6 
0.4 
0.2 

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Takeshi t a 



Shono 



Arakawa 



Figl7.8 Estimated doses for Nishiamaites in Sv. 

Bomb Dosimetry and Dose Groups 

Till 1957, survivors were grouped on the basis of twin criteria of (a) distance from 
the hypocenters at the time of bombing (ATB) and (b) history of symptoms of acute 
radiation syndromes like loss of hair, bloody diarrhea etc. The first dosimetry in 
which all survivors within 2000 meters from the hypocentres were allotted their 
individual doses was created in 1957. Since then, there have been four revisions. 
Initially, the exposed group consisted of survivors who were within a radius of 2,000 
meters from the hypocentres. Those who were beyond 10,000 meters from the 
hypocentres, labeled as 'Not-In-City (NIC) ATB', were treated as the unexposed 
control group. NIC included two sub-cohorts: (a) the residents who were 
temporarily away from the cities ATB and (b) the immigrants from other prefectures 
and expatriates from the oversea colonies who settled down in the cities after the 
bombings and before the initiation of the study. Many among group (a) above 
returned to the cities immediately after the bombs and participated in search, rescue 
and rehabilitation works. They were exposed to residual radiations from NAP and 
some of them experienced symptoms of acute radiation. Recognizing this, the 
government classified the people who returned to the cities within 15 days of the 
explosions as bomb survivors under the Atomic Bomb Survivors' Medical 
Treatment Law of 1957. ABCC did not bother to remove the exposed early entrants 
from NIC. Since there were differences in income and health status between the 
expatriates and the resident population, ABCC treated NIC as the 'external' control 
group and carved out an 'internal' control group consisting of residents who were 
beyond 3,000 meters from the hypocenters ATB. As the latter had received some 



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ECRR Proceedings Lesvos 2009 

prompt radiations from the bombs, estimated to be less than 5 milliSievert (mSv), it 
is also known as the distally exposed (DE) group. 

Besides the prompt radiation, some residents in the fall-out areas located 
beyond 3 km were exposed to chronic external and internal radiations from fission 
products and bomb debris. In other words, both the internal and external control 
groups included subjects who were exposed to residual radiations. The radiation 
measurements at the hypocenters and the fall-out areas were not incorporated in the 
bomb dosimetry. As we shall see later, this 'contamination' has seriously 
jeopardized the results of the health studies. (Fig 9) 

Between the years 1950 and 1981, ABCC/RERF researchers published 10 
papers on SR as journal articles and technical reports. All the papers published 
before 1965 highlighted the pro-genetic theory deviations in SR during 1948-53. 
One paper had a provocative title- "Sex ratio among children of survivors of atomic 
bombings suggests induced sex-linked lethal mutations" [10]. This position was 
reversed and the question of bomb radiation causing visible and measurable 
genomic changes was settled forever in 1981. 

In order to see if the reversal of the results is real, I compared the data 
published in 1965 and 1981. Since each revision in dosimetry also involves inter- 
group shifting of survivors, comparison of dataset is problematic. Since the subjects 
in NIC group were not affected by the revisions, their numbers should be the same 
in all reports. For the comparison of data, we have used two groups - NIC and 
Exposed, the latter comprises of proximally (<2000 meters) and distally (3000- 
10000 meters) exposed persons. There are four groups in this comparison; (i) both 
parents NIC, (ii) both exposed, (iii) mother exposed and (iv) father exposed. Data 
on children born during the two phases as given in 1965 and 1981 reports are in the 
data appendix [*]. 



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ECRR Proceedings Lesvos 2009 

CONTROL GROUPS IN BOMB 
EFFECT STUDIES 

THERE WERE 2 CONTROL GROUPS IN ALL STUDIES OF ABCC 

1. 10KMAWAYFROMHYPOCENTRES ATB - EXTERNAL 
CONTROL GROUP - LABEL = NIC ATB 

2. RESIDENTS BEYOND 3 KM FROM HYPOCENTRES - KNOWN 
INTERNAL CONTROL GROUP - LABEL = DISTALLY EXPOSED 

BOTH INCLUDED EXPOSED PERSONS 

EXPOSURE DETAILS OF NIC 

NIC ATB (10 KM AWAY FROM GROUND ZERO) 

RESIDENTS, TEMPORARILY AWAY ATB, 

RETURNED ASAP IN SEARCH OF RELATIVES. 

EXPOSED TO RESIDUAL RADIATION FROM NEUTRON ACTIVATION 
PRODUCTS 

INCLUSION OF EXPOSED IN CONTROL GROUP 

• 1967 -GOVT CONSIDERS PEOPLE RETURNING TO THE CITIES 
WITHIN 15 DAYS OF BOMBS (NIC EARLY ENTRANTS) AS BOMB 
SURVIVORS. 

• 20% OF NICS IN ABCC SAMPLES WERE EARLY ENTRANTS. 
SOME OF THEM HEAVILY EXPOSED. 

INTERNAL CONTROL GROUP - SURVIVORS > 3 KM FROM GROUND 
ZERO 

• WITHIN SIX HOURS AFTER DETONATION, BLACK RAINS OF 
FISSION PRODUCTS IN OUTSKIRTS OF BOMBED CITIES - 3 KMS 
AWAY FROM GROUND ZEROS. 

THIS CONTROL GROUP INCLUDED PEOPLE LIVING IN FALL OUT AREAS 
ALSO 

Fig 1 7.9. The controls groups for the radiation genetic studies 



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ECRR Proceedings Lesvos 2009 

In Phase I there were 70,212 births as per 1965 report and 70,082 births as 
per 1981 report. The second report is short 103 boys and 27 girls. Besides this 
exclusion, there were shifts between exposure groups. In the 1981 report 490 
children were removed from NIC-NIC and father-exposed groups, while 360 
children were added to mother-exposed and both-exposed groups. After these 
modifications, SR of the entire cohort declined from 1078 in 1965 report to 1075 in 
1981 report. All the exposed groups also underwent such marginal changes. 
As per the 1981 report, 72,902 children were born in Phase II and their SR was 
l,100(df =1, chi sq 49.44, p= 0.0000). SR was even higher (1,132) among the 
39,995 children born to proximally and distally exposed parents (df =1, chi sq 49.44, 
p= 0.0000). Likewise, during the first phase SR of the total sample and NIC-NIC 
cohort was significantly higher than the Japanese SR. Changes are changes, even 
though they do not follow the theories. RERF has a responsibility towards their 
subjects to probe the reasons for the observed difference. 

In the data for phase II (1954-65), 1819 boys and 753 girls were added in 
the 1981 report. Boys were added to all the four cohorts. 856 girls were added to 
NIC-NIC and father-exposed cohorts, while 103 girls were removed from mother- 
exposed and both-exposed groups. SR for all children born during 1954-65 was 
1071 in 1965 report and 1100 in 1981 report as more boys than girls were added. 
NIC-NIC group's SR declined from 1070 in the 1965 report to 1063 in the 1981. 
There were increases in SR in the other three cohorts. SR of two groups is above 
1,150, incredibly high ratios, not reported in any normal population so far. In a long 
term epidemiological study involving large number of events, data cleaning and 
removal of bad data is inevitable. In such a situation, the authors have to give 
convincing arguments supporting the changes. The data modifications are not 
mentioned in the 1981 paper. Total number of children added for 1954-65 is 2,572 
and its impact on SR of all cohorts is very high. As the changes for the period 1948- 
53 is minimal and the impact on SR marginal, this reanalysis is confined to Phase I 
data only. 

Reanalysis of SR data for 1948-53 

In TR-7/81, there are five dose groups - NIC, <5 mSv, 5 mSv to 0.1 Sv, 0.1 - 1 Sv 
and <1 Sv. (1 Sv = 100 Rem). The first two groups represent the external and 
internal control groups respectively. Considering the exposure of both parents, there 
are 25 exposure groups in the analysis. Of the 70,082 children in the study, 83% 



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ECRR Proceedings Lesvos 2009 

were born to parents in four 'control' groups - NIC-NIC = 49%, NIC-DE/DE-NIC = 
26% and DE-DE = 8%. That leaves 1 1,914 children of exposed parents to be placed 
in 21 cells. Since the chance of being born as a boy or a girl is (almost) 50-50, large 
numbers of births are required for detecting any real change in SR. The data under 
consideration simply do not permit disaggregation into 21 exposure groups. 
Therefore we have compressed the dose groups into three, - NIC, <5 mSv and 5 
mSv+, corresponding to the external control group, the distally exposed (DE) 
internal control group and the proximally exposed (PE) group respectively. When 
the exposures of father and mother are considered, there are nine dose groups. The 
results are given in Fig 10. 

I REDUCED THE EXPOSURE GROUPS INTO THREE 

• NIC - EXTERNAL CONTROL 

• DISTALLY EXPOSED - INTERNAL CONTROL 

• PROXIMALLY EXPOSED - ALL SURVIVORS <2.5 KM 

• THERE ARE NINE PARENTAL DOSE GROUPS IN THIS 
RE ANALYSIS 

DEVIANT SR IN CONTROL GPS 

• SR OF CONTROL GP 1 (NIC-NIC) = 1089 

• SR OF CONTROL GP 2 (DE- DE) = 1034 

• SR OF ALL JAPANESE KIDS = 1055 

• SR IN MAJOR COUNTRIES = 1050 - 1065 

Fig 17.10 Reanalysis of the sex ratio studies 

SR of the two control groups- DE-DE and NIC-NIC - are 1034 and 1089 
respectively. It is strange that the scientists at ABCC/RERF did not pay any 
attention to this difference between the two control groups. Because of this gross 
difference between the 'control' groups, I have considered all children born to 
Japanese nationals in Japan as the reference group. There were 19,427,142 births in 
Japan during 1950-55; their SR was 1055 [11]. (Japanese SR increased to 1,066 
during 1970-74 and decreased to 1,057 during 1990-94 [12]. Incidentally, during 
the second half of the 20th century all major countries with reliable birth statistics 
had SR in the range of 1050-1065 [13]) In this discussion Japanese SR is considered 
as the reference; ratios lower and higher than it will be deemed as female excess and 
male excess respectively. The male excess cohort would have experienced loss of 



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female zygotes due to dominant lethal mutations in the sperms and the female- 
excess cohort would have experienced loss of male zygotes due to recessive lethal 
mutation in the ova. The numbers of boys and girls 'missing' from the cohorts are 
given in columns (i) and (j) respectively. (If these 'missing' girls and boys were 
added to the cohort, their SR would be 1055). The estimated percentage of zygotes 
that could have been lost due to lethal mutation on X chromosome is given in 
column (m). To estimate this, the boys/girls born and 'missing' has been used as the 
denominator. 

Results 

Five exposure groups had excess of females and four have excess of males in 
comparison with the Japanese SR. In the female excess cohorts, the mothers were 
proximally exposed in three, were distally exposed in one and were NIC in one 
cohort. At the same time, the fathers were proximally exposed in one group, NIC in 
one and distally exposed in three groups. In the four male excess groups, the fathers 
were proximally exposed in two and NIC in the other two cohorts. The mothers 
were distally exposed in two and NIC in two groups. The percentage male in total 
births in the study during 1948-53 is 51.82 as against the reference percentage of 
51.34 in Japan and the difference between them is statistically significant (df=l, p= 
6.36, chi sq =0.012). Within the groups, the proportion of male in offspring of NIC- 
NIC couples is 52.12 and this difference is also highly significant. (df=l, p= 8.54, 
chi sq = 0.0034). An estimated 230 male zygotes and 869 female zygotes were lost 
from the female excess and male excess cohorts respectively. These represent 2.5% 
of the male zygotes and 3.3% of the female zygotes conceived during 1948-53. 

The main findings of this reanalysis are: 



• 



There has been an arbitrary, sex selective addition of data in the paper 
published in 1981. This has masked the effect on SR reported earlier. 

• SR of both the internal and external control groups differs from the 
reference SR. 

• There is a significant increase in SR in the total sample of the Phase I. 



• 



SR of all the nine cohorts is different from the Japanese SR. The highest 
aberration (male excess) is found in the children of NIC fathers. The 
offspring of distally exposed mothers have a lower SR (Fig 11, 12). 



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THE MAIN FINDINGS OF THIS REANALYSIS 

• Arbitrary, sex selective addition of data in the 1981 
paper masked the effect on SR. 

• SR of both internal and external control groups 
differs from the reference SR. 

• The highest male excess is in children of NIC fathers. 

• The distally exposed mothers have a lower SR. 

• Significant increase in SR in total sample of Phase I. 

• SR of all the nine cohorts is different from the Japanese SR. 



Fig 17.11 The main results of reanalysis of the data 

MAEDfflQT-EXPOSffiMOTHKS MAIEEXCESS- EXPOS© FATHBB 




Fig 17.12 Deficit/ excess of males per 1000 females 1948-53 

Discussion 

In three out of the five female excess cohorts, mothers were proximally exposed and 
in two out of the four male-excess cohorts fathers were proximally exposed to 
instantaneous radiation from gamma rays and neutrons. The female excess could 
have been due to loss of male zygotes carrying a maternal X chromosome with 
recessive lethal mutation. Likewise, the male excess may be due to dominant lethal 



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mutation in the paternal X chromosome. These five experiences are pro-genetic 
theory. In the other two female excess cohorts, mothers were distally exposed in 
one and NIC in the other. Likewise, in the other two male-excess groups, the fathers 
were NIC. These aberrations could have been due to the inclusion of persons 
exposed to residual radiation from fall-out and NAP in the distally exposed and NIC 
groups. If this factor is taken into consideration, the changes in SR in all the nine 
cohorts in this analysis could be considered as radiation-induced and are pro-genetic 
theory. 

Other Human studies on SR 

The publication of preliminary results by ABCC in 1952 caused a flood of reports 
on radiation and birth SR by several scholars. Results of 18 series of post- 
irradiation births (9 father exposed and 9 mother exposed) are availabe [14]. This 
includes two series in which the parents were in utero ATB in the target cities. The 
sample sizes in all the individual series, except that of the US and Japanese 
radiologists are too small. All the authors used another small, unexposed group for 
comparison and some of which were different from the national SR. For instance, 
SR of all births in US during the fifties was 1050, SR of radiologist's children's was 
1,057 and SR of the children of physicians in other specialties was 1,125. There 
appears to be something wrong with the data of physicians who were not 
radiologists. In this review, the SR in their respective countries during the period of 
study is used as the reference. The offspring SR in two out of nine series of paternal 
exposure -Czech miners and French patients- is lower and is contra-theory. SR of 
US radiologists' children does not differ from the national SR. In the remaining six 
series, there is an increase in male birth. The difference is statistically significant in 
the case of Japanese radiologists (chi sq 12.59, p= 0.003). If all the offspring of 
exposed fathers are brought together, the proportion of male is 52.38% and this is 
significantly different from the estimated mean proportion of 51.35% (chi sq 5.1 1, p 
= 0.0238). In the case of maternal exposure, all groups other than the Japanese in 
utero series show male deficit and are hence pro-theory. If all data of the children 
born to exposed mothers are combined, the difference is significant (chi sq 6.29, p= 
0.0121) (Fig 13). 



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WHBM FATHHREXPOSH) 



WHBM MOTHBREXPOSBD 



1500 
1400 
1300 
1200 
1100 
1000 



1. 



Ill 



8 S | 
* * jjj 



13 




Fig 17.13 Sex ratio after therapeutic radiation studies 

The Effects of Chronic Exposure 

Most of the bomb survivors and the subjects of studies listed in table 3 received 
acute radiation either from the bombs or from the clinics. In the case of GE-3 study, 
there was a gap of about 20 to 80 months between the exposure and the conception. 
The target of exposure in this case is spermatogonial (stem) cells. In a situation of 
chronic exposure, besides the stem cells, the cells undergoing division are also 
exposed. Results of three studies of birth sex ratio of children born to parents 
exposed to chronic low dose radiation are summarized below. 

In a retrospective cohort study of 260,060 singleton births between 1950 
and 1989 to mothers resident in Cumbria, north west England, Dickinson et al 
observed that the SR among children of men employed at any time at Sellafield 
plutonium processing plant was 1.094 (95% CI: 1060, 1.128), significantly higher 
than that among other Cumbrian children, 1055 (95% CI: 1.046, 1.063). SR of 
children whose fathers were estimated to have received more than 10 mSv of 
radiation in the 90 days preceding conception was even higher at 1396 (95% CI: 
1.127, 1.729) [15] (Fig 14) 



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EXCESSMALESPER1000 FBVIALES 


450 -| 




400 


^ m 


350 - 




300 




250 




200 


m _ 


150 




100 
50 - 
- 


.■III 


Normal SR Sellaf ield 1 Sellaf ield 2 BARC, India TAPS; India 



Sellafield 1 = All Workers (1950-1989) 

Sellafield 2 =90 days B4 conception 

BARC, India = 1960-1984 
TAPS, India =1970-1994 

Fig 1 7.14 Sellafield workers study 



Scherb and Voigt conducted the largest sex ratio study of 25 million births during 
1984 to 1992 in eight European countries (Czech Republic, Denmark, Finland, 
Hungary, Norway, Poland, and Sweden and Germany). They found a uniform 
downward trend of the male birth proportion from 1982 to 1986 and a sudden 
increase in 1987 with an odds ratio of 1.0047 (1.0013-1.0081, p = 0.0061). The 
authors attribute the shift in 1987 to the radiation exposure from the 1986 accident at 
the Chernobyl nuclear reactor [16]. 

A study of 31,569 children born to the workers of the Bhabha Atomic Research 
Centre (BARC) and the Tarapur Atomic Power Station (TAPS) during the years 
1956-1994, also shows significantly higher proportion of male, which cannot be 
explained by any other factor. In BARC, SR of 1960-1984 cohort was 1205. When 
compared with the reference SR of 1060, there is a significant excess of male in 
BARC (df=l, Chi sq =68.93, p=0.00000) and TAPS (df=l, chi sq=10, p=0.00165) 
[17]. 



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Manipulated data and an untested theory 

The proposal for the genetic study in the bombed cities was made by James V Neel, 
a US naval officer, who served with ABCC. He and his colleague William Schull of 
the Department of Human Genetics, University of Michigan Medical School, were 
co-authors in all the papers dealing with SR. In spite of their 'negative' findings, 
these authors believe that "genetic damage did occur because of the radiation 
exposure." [18]. Ernest Sternglass quotes from a lecture by Neel in 1963: "in view of 
the vast body of data regarding the mutagenic effects of radiation, it can scarcely be 
doubted that the survivors of Hiroshima and Nagasaki sustained genetic damage. 
The question is not 'Is there damage?' but rather "Can the damage be detected?'" 
[19]. 

Change in SR was the first demonstrated effect of radiation induced 
mutations. Since Herman Mueller's historic experiment in 1927, the effect has been 
repeated in several test systems. Now we have a fairly large series of human data 
also from bomb survivors, radiation workers, down-winders and people exposed to 
the Chernobyl fallout. Commenting on the sex ratio study of Sellafield workers, WH 
James, an expert on birth sex ratio says: "as far as I know, ionizing radiation is the 
only reproductive hazard which causes men to sire an excess of sons" [20]. At the 
same time, Neel and co-authors from RERF propose a new hypothesis on sex-linked 
lethal mutation, based on the observation that one of the X chromosomes in the 
somatic cells of the mammalian female is inactivated - a process known as 
Lyonization. They argue that since one X chromosome in the somatic cells of the 
female is inactivated, "it became clear that sex-linked mutations induced in males 
were unlikely to have a dominant lethal effect in females" [21]. This implies that a 
female zygote would have a normal and complete life, even with only one X 
chromosome. RERF website also claims that "given these developments, most 
human geneticists no longer accept the simple, early arguments, and contend that 
prediction of the effects of lethal mutations on the frequency of male births is not 
possible" [22]. 

Lyonization or methylation of one of the two X chromosomes in the female 
has been known for over three decades. However, lyonization does not involve 
complete silencing of all the genes. According to Carrel and Huntington, about 25% 
of the genes on the 'lyonized' X chromosome, most of them in the pseudo- 
autosomal region (PAR), are not inactivated [23]. In other words, the second X 
chromosome or at least its un-silenced genes are necessary for the normal growth 



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and development of the female. Some girls are born with one X chromosome only 
(45X0), a condition known as Turner syndrome. They are severely handicapped 
and are infertile. About 98% of the 45X0 zygotes are lost before term. Birth 
incidence of 45 XO is 4/10,000 births. For all practical purposes, 45 XO can be 
considered as the product of a dominant X-linked lethal mutation. This reanalysis 
shows that 869 girls were missing from the four male-excess cohorts with a total 
birth of 52,616. There could have been 21 45X0 girls in the above cohorts. These 
and the missing girls might have inherited a lethally mutated X chromosome. 

The Universe and the Samples 

In an epidemiological study, there are samples that are representative of the 
universe. When the samples for GE-3 studies were assembled, the two control 
groups - NIC and DE represented not only the victims, but also of the aggressor. 
The soldiers who were marched to occupy the conquered lands, the scientists who 
were to assess the impacts of the new weapons and the doctors and other social 
workers who went there to heal the wounds were NIC. Likewise, there were 
'distally exposed' people in USA also. Twenty one days before the bombing of 
Hiroshima, the Gadget, the first atom bomb in the trinity test series with an 
estimated yield of 21 KT was exploded in New Mexico. The fall-out plume was not 
tracked; there is no documentation about the distally exposed cohorts there. The 
workers, down- winders and down- streamers of the Hanford pile and other facilities 
have been living with the fission products five years before the explosions. All 
these people were also 'distally' exposed. In short, there was a conflict of interest in 
all the health studies conducted in the bombed cities. I had personal and group 
interactions with the members of Fl generation in Hiroshima and Nagasaki during 
the 1990's. They were not interested to discuss the genetic effects of ionizing 
radiation. This is understandable. People do not want to be told of a permanent and 
irreversible change in their genome. So, in the bomb cities, the epidemiologists and 
their subjects had a vested interest in not seeing the genetic effects. Today, sixty 
four years after the bombings, the universe of the ABCC-RERF studies consist of all 
of us on the planet. Nuclear weapon tests, accidents at Chernobyl, Three Mile 
Island and Sellafield and routine releases from nuclear power plants have released a 
million times more radionuclides into the environment. 



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Conclusion 

Incidentally, ABCC-RERF studies have almost all the features of a prospective 
epidemiological study and have large number of exposed persons of both sexes. 
RERF's negative 'findings' dampened the interest of a generation of workers in 
radiation genetics. The reports of RERF, the biggest health research facility on 
earth, are considered as the final word by the radiation standard setting agencies like 
the Biological Effects of Ionizing Radiation (BEIR) committee of the US National 
Academy of Sciences and UNSCEAR. Even after the intense exposure to ionizing 
radiations for three generations from making and testing of bombs and operation of 
nuclear power plants, the United Nations' Scientific Committee on Effects of 
Atomic Radiation (UNSCEAR) claims "no radiation-induced genetic diseases have 
so far been demonstrated in human populations exposed to ionizing radiation."[24]. 
So powerful is the influence of RERF that even researchers who report strong 
positive association like Dickinson and co-authors think that the "studies of the 
possible association between parental preconceptional irradiation and an altered sex 
ratio do not yet satisfy the Bradford Hill criteria for inferring a causal relationship 
[25]. All because, the final word has been pronounced by RERF. A proper 
reanalysis of all the genetic studies conducted by ABCC and RERF will 
undoubtedly reveal the true impact of radiation on the gene and our ignorance about 
us. 

References 

1 Muller, H.J. (1927) Artificial transmutation of the gene. Science 46: 84-87. 

2 World Health Organization, 1957. Effects of Radiation on Human Heredity: 
Report of a Study Group p 87 

3 COMARE, Fourth Report, 1984, The incidence of cancer and leukemia in young 
people in the vicinity of Sellafield site, West Cumbria 

4 Sperling, K., J. Pelz, R-D. Wegner et al. 1994, Significant increase in trisomy 21 
in Berlin nine months after the Chernobyl reactor accident: temporal correlation or 
causal relation? Br. Med. J. 309: 158-162. 



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5 VT Padmanabhan, AP Sugunan, CK Brahmaputhran, K Nandini and K 
Pavithran, 2003, Heritable anomalies among the inhabitants of regions of normal 
and high background radiation in kerala: results of a cohort study, 1988— 

1994, International Journal of Health Services, 

6 Neel JV, Schull WJ, McDonald DJ, Morton NE, Kodani M, Takeshima K, et al.. 
(1953) The effect of exposure to the atomic bombs on pregnancy termination in 
Hiroshima and Nagasaki : Preliminary Report. Science, 118, 537-541. 

7 Neel JV, Schull WJ,(1981), RERF TR 7/81 

8 UNSCEAR, 2000 Annex C , table 1 

9 Arakawa ET. (1962) Residual radiation in Hiroshima and Nagasaki. ABCC TR- 
IO To be added 

1 1 United Nations. Demographic yearbook, 17th edition (1965). 

12 Parazzini F; La Vecchia C; Levi F; Franceschi S. (1998) Trends in male-female 
ratio among newborn infants in 29 countries from five continents. Hum Reprod. 13, 
1394-6. 

13 United Nations. Demographic yearbook, 38th edition (1986). 

14 Schull WJ, Neel JV, Hashizume A. (1965) Further observations on sex ratio 
among infants born to survivors of the atomic bombs. ABCC TR 13: p 12. 

15 Dickinson HO, Parker L, Binks K, Wakeford R, Smith J. (1996) The sex ratio of 
children in relation to paternal preconceptional radiation dose: a study in Cumbria, 
northern England. J Epidemiol Community Health. 1996; 50(6):645-52 (ISSN: 
0143-005X) 

16 Scherb H and Voigt K (2007) Trends in the human sex odds at birth in Europe 
and the Chernobyl Nuclear Power Plant accident. Reproductive Toxicology 23, 593 
599. 

17 VT Padmanabhan, (2009) Offspring sex ratio of Indian nuclear workers 
suggestive of radiation induced genetic changes, (Unpublished) 

1 8 Genetic effects and birth defects from radiation exposure, Hanford Health 
Information Network, 

http ://www.doh. wa. gov/Hanford/publications/health/mon8 .htm , accessed on 07 
April 09 

19 E Sternglass, http://www.ratical.org/radiation/SecretFallout/SFchp6.html 

20 W H James 1997, Ionizing radiation and offspring sex ratio, J Epidemiol 
Community Health. 51(3): 340-341. 



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21 A Review of Forty-Five Years Study of Hiroshima and Nagasaki Atomic Bomb 
Survivors The Children of Parents Exposed to Atomic Bombs: Estimates of the 
Genetic Doubling Dose of Radiation for Humans James V. Neel, William J. Schull, 
Akio A. Awa, Chiyoko Satoh, Hiroo Kato, Masanori Otake and Yasuhiko 
Yoshimoto, (1991) J. Radiat. Res., Supplement, 347-374 

22 Were more boys or girls born to atomic-bomb survivors?, 
http://www.rerf.or.jp/radefx/genetics e/sexratio.html (Accessed on 15 April 09) 

23 L Carrel & HF. Willard, 2005, X-inactivation profile reveals extensive 
variability in X-linked gene expression in females, Nature 434, 400-404 

24 UNSCEAR 2001 Report, Summary and conclusions, Annex: hereditary effects 
of radiation, page 83 

25 Dickinson HO, Parker L, Binks K, Wakeford R, Smith J.et al, 1997, Ionizing 
radiation and offspring sex ratio, J Epidemiol Community Health. 51(3): 340-341. 

* Data appendix: the tables of data from the reanalysis are available from 
admin(£)euradcom.org 



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18 
Underestimation of genetic and somatic effects of 
ionizing radiation among the A-bomb survivors in 
Hiroshima-Nagasaki 

VT Padmanabhan 

vtpadma@gmail.com 

Introduction 

In August 1945 two fission devices exploded in the morning skies of Hiroshima and 
Nagasaki with the 'brightness of a thousand Suns' and explosive energy equivalent 
to 36,000 tons of TNT. 1. These generated heat blast and ionizing radiations (IR). 
The sources of IR were gamma rays (photons), neutrons, neutron activation products 
(NAP), fission products (FP), and micro/nanoparticles of unfissioned 235uranium 
(23 5U) and 239plutonium (239Pu). The photons and neutrons caused prompt 
exposure within seconds in an area with radius of about 2,500 meters of the 
hypocenters (OTH). Radioactive particles like NAP, FP and other radioactive 
particles contaminated the soil and water bodies and the food web. Besides the 
external radiation, these were also sources of chronic internal radiation through 
inhalation and ingestion. NAPs are radioactive species like 14carbon and 3tritium 
formed when neutrons interact with the nuclei of stable atoms of nitrogen and 
hydrogen. Out of 50 kg of enriched uranium in the core of Hiroshima bomb, only 
855 grams were fissioned. Out of an estimated 15 kg of Pu in the Nagasaki bomb 1.2 
kg was fissioned. Fission products are nanoparticles with radioactive half lives 
ranging from seconds to millions of years. FP yields were 4.35x1024 atoms in 
Hiroshima and 6.09x1024 atoms in Nagasaki. The estimated yields of NAP were 
about half that of the FP. Within an hour of detonation, part of the bomb debris 
containing radioactive particles fell in the outskirts of the cities and the rest was 
lofted to the stratosphere. These particles were found in the ice core drilled from the 
Arctic ice caps as well as in the samples of soil, sediment, and tree rings from fall 
out areas in Japan. Hiroshima-Nagasaki events have been billed as the first major 
global circulation experiment.2 (Please see supplementary table 1 for the physics of 
the bombs) 



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Residual Radioactivity near the hypocentres and in the fallout areas 

The Atomic Bomb Casualty Commission (ABCC) was constituted in 1945 to study 
the impacts of the bombs. ABCC conducted studies of radiation effects till 1975. 
The Radiation Effects Research Foundation (RERF), set up with financial support 
from the governments of USA and Japan took over the assets and programmes of 
ABCC. Measurements of residual external radiation near the hypocentres and the 
fallout areas were done by Japanese and US scientists within days of the events. In 
the dosimetry report published by ABCC 14 years after the study, the authors lament 
about the ordinary people's ignorance of residual radiation. 3 The FP fallout areas 
were Koi Takasu, 3 km west of Hiroshima and Nishiyama, 2.8 km east of Nagasaki. 
Studies of concentration of plutonium, cesium, and strontium in soil, sediment and 
tree rings from the hypocentres and fall-out areas sampled during 1980s bear 
signatures of the devices. The concentration 239/240 Pu at 2.8 km was 1800 Becquerel 
per square meter (Bq/m 2 ), thirty times higher than the total Pu fall-out in Japan from 
all nuclear weapon tests during 1945-64. Concentration of 137 cesium was 5260 
Bq/m 2 , seven times higher than the deposition at Washington County that received 
the highest fallout from all weapon tests at Nevada, USA. (Supplementary table 2 
for contamination details) 

Dose Groups in epidemiological studies 

In the epidemiological studies, the survivors who were within 2,500 meters OTH at 
the time of bomb (ATB) were considered as the exposed group. Distance from 
hypocentres, shielding by structures, and history of symptoms of acute radiation 
were the criteria for dose-grouping. There were two control groups in the studies, 
i.e. (i) Not In City (NIC) ATB consisting of subjects who were beyond 10,000 
meters OTH and (ii) the Distally Exposed group consisting of residents who were 
between 3,000 -10,000 meters OTH ATB. DS02, the newest bomb dosimetry 
adopted in 2002 assigns a dose of 5 milliSievert (mSv) to the distally exposed 
(Control) and 10 mSv and above to the proximally exposed subjects. Eighty percent 
of the NIC group consisted of immigrants from other prefectures and overseas 
dominions who came to the cities when rebuilding activities started a couple of 
months after the events. The rest of the NIC were residents who were temporarily 
away from the cities ATB and had returned to the cities as early as they could. They 
participated in search and rescue operations near the hypocentres and were exposed 
to residual radiation. Many of them experienced acute radiation syndromes. People 



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who entered the cities within 14 days of the explosions were treated as bomb 
survivors under the Atomic Bomb Survivors Medical Treatment Law (ABSMTL) 
1957 4 . These people and the residents under the fallout cloud in the distally exposed 
cohort were exposed to internal and external radiations. 

In response to ABSTML, ABCC split the NIC group as NIC Early Entrants 
(EE) and NIC Late Entrants (LE). NIC EE consisted of subjects who entered the 
cities within 30 days of the bombings. In spite of this bifurcation, the combined NIC 
group is still considered as the control group in all the genetic studies and some of 
the somatic studies being conducted by RERF. The labels 'early entrants' and 'late 
entrants' cannot be found in any report of RERF. This paper is a review of genetic 
and somatic effects of the bombs. On the genetic effects, two papers of the SR study 
published in 1965 and 1981 are compared and reanalyzed. The reappraisal of 
somatic effects is based on the 1973 LSS report authored by Moriyuma and Kato 
which provided separate mortality data for NIC EE and LE for the first and the last 
time. 

PART I - SEX RATIO - ABERRATIONS IN THE CONTROL GROUPS 

Radiation-induced dominant lethal mutation in male X chromosome and recessive 
lethal mutation in female X chromosome will lead to deficit of girls and boys 
respectively in the progenies conceived after the exposure. This was demonstrated 
experimentally by HJ Muller in fruit flies in 1927.5 In 1965 Schull et.al 
summarized the results of 16 studies of 13,511 children conceived after exposures. 6 
In eight of these, the mothers and in the remaining eight the fathers were exposed at 
the workplaces or in the clinics. When compared with the national birth SR, the 
findings in 14 studies were pro genetic theory. In recent times, change in SR has 
been observed in children of workers of the plutonium processing plant at 
Sellafield7 and in Chernobyl- contaminated Europe8. In view of the increasing 
threat to the genome from environmental mutagens, Davis et al suggested that birth 
SR be treated as a sentinel health indicator. 9 

ABCC study of 70,212 children born during 1948-53, showed a male deficit in 
exposed mothers' offspring (p <0.05) and female deficit in exposed fathers' 
offspring. 10 Since these findings were pro-genetic theory, the second phase SR 
study was conducted during 1954-62. The report of the extended study of 140,252 
children born during 1948-62 was published in 1965.6 The last report of this study 
published in 1981 after a revision in dosimetry concluded that the results of 1948-53 
and 1954-62 were opposite in direction and the positive effects reported earlier was 
fortuitous and irrelevant for the radiation debate. 1 1,12 



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Comparison of the reports published in 1965 and 1981, (given in supplementary 
table 3) reveals sex selective changes in database in the 1981 report. During 1948- 
53, there were 70,212 births (SR =1,078) in 1965 report and 70,082 births (SR = 
1075) in 1981 report. 103 boys and 27 girls were missing in the 1981 report. Total 
birth and SR during Phase II were 70,330 (SR= 1,071) in 1965 report and 72,902 
(SR=1,100) in 1981 report. In the 1981 report, 1819 boys and 753 girls were added 
to the database. Boys were added in all cohorts except the NIC-NIC. Total children 
in the database for both phases according to 1965 report were 140,542 and SR was 
1,074. The number increased to 142,984 and SR increased to 1,088 in 1981 report. 
Since the number given in two subsequent reviews authored by Neel and Schull in 
199113 and Nakamura in 200614 is 140,542, it seems that the 1981 data was 
incorrect. The data error and the conclusions of 1981 report have not been corrected 
so far. 

Reanalysis of 1948-53 SR data 

Since the change in database and its impact on SR is modest for 1948-53, I have 
reanalyzed this data as published in 1981. In RERF report, there were five dose 
groups - NIC, <5mSv (Distally Exposed) and three proximally exposed groups with 
dose ranging from 10 mSv to 2000 mSv. More than 75% of the children were born 
to the 'unexposed' parents in four parental groups and there are fewer than 50 
children in many of the remaining 21 groups. Since the chance of being born as a 
boy or a girl is almost 50-50, large number of birth is required for detecting any real 
deviation in SR. The data under consideration do not permit disaggregation into 25 
cells. To reduce the number of cells, I have compressed the dose groups into three 
as - NIC, Distally Exposed and Proximally Exposed. (Table 1). SR and proportion 
male (male birth/total birth) are given in columns (f) and (g). Estimated number of 
lost zygotes that resulted in the deviant SR is given in columns (h) and (i). 

Results 

SR of the total sample is 1975, as against the background SR of 1955. This 
difference is statistically significant. (p= 0.0117). Of the nine groups in this 
analysis, five are male-deficit and four are female deficit. The group in which both 
the parents were proximally exposed (row 1) had the lowest SR of 968. Offspring of 
proximally exposed fathers and NIC mothers registered the highest SR of 1146. 
Though these are wide off the background sex ratio, they are not statistically 
significant. Nearly half the children in the study were parented by NIC-NIC couple 
(row 7). Their SR was 1089 and this significantly different from the background 
SR. (p= 0.0034). 



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DISCUSSION 

Genetic effects 

The number of children born to people exposed to the prompt radiation (proximally 
exposed group) was small. Hence, the SR study did not reveal any significant 
difference. The total sample in the study exhibits a statistically significant male 
excess in comparison with the Japanese national SR. This is mainly due to the male 
excess in the two comparison groups (rows 6 and 7) in which fathers were NIC. Of 
these two groups, offspring SR of NIC-NIC (row 7) couples is statistically 
significant. In the absence of any other competing hypothesis, it is likely that the 
high maleness in this group and also the other group (distally exposed mother and 
NIC father at row 6) is due to the exposure of some fathers to residual radiations. 
There is however, no visible impact of exposure on the offspring of NIC mothers. 
This may be because of the fewer number of females among the NIC Early Entrants 
and also due to the sexual division of labour prevalent in Japan during the Second 
World War. 

This is the first attempt to assess the risk of IR induced somatic and genetic effects 
in the bomb survivors in one analysis. Within eight years of exposure, control 
groups in the genetic study exhibited mutation-induced loss of pregnancies. They 
also started dying earlier, which became statistically visible within 27 years post 
bombing. These findings from two different studies are complementary to each 
other. In the absence of any other known risk factor, these excesses can be 
attributed to exposure to residual radiations. 

Assuming that the changes in SR are due to X-linked lethality, 230 male and 869 
female zygotes (0.6% and 2.6% of the total boys and girls in the study) were lost 
from the cohort. Out of 20,252 identified genes in the human genome, 5.6% are 
located on the X chromosome. 18 Since there are lethal genes on autosomes also, the 
total zygotic losses would have been much higher. Likewise, the exposure could 
have caused detrimental mutations as well, which may be visible after a reanalysis 
of other endpoints in GE3 study with a realistic dosimetry. Since the NIC and the 
distally exposed cohorts serve as the control groups in all other genetic studies 
conducted by RERF, this reanalysis has implications for all of them. 



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ECRR Proceedings Lesvos 2009 



Row 


Exposure Status of 


Male 


Female 


SR 


Proportion 


Missing 


Missing 


ChiSq 


P 


No 


Mother 


Father 








Male 


Boys 


Girls 






(a) 


(b) 


(c) 


(d) 


(e) 


(f) 


(g) 


(h)* 


(0* 


0) 


CO 










1948-53 














1 


Proximal 


Proximal 


762 


787 


968 


49.19 


68 




2.86 


0.0909 


2 


Proximal 


NIC 


2959 


2891 


1024 


50.58 


91 




1.35 


0.2456 


3 


Distal 


Distal 


2816 


2724 


1034 


50.83 


58 




0.58 


0.4479 


4 


Proximal 


Distal 


582 


556 


1047 


51.14 


5 




0.02 


0.8938 


5 


NIC 


Distal 


1736 


1653 


1050 


51.22 


8 




0.02 


0.8934 


6 


Distal 


NIC 


7747 


7115 


1089 


52.13 




228 


3.69 


0.0546 


7 


NIC 


NIC 


17785 


16332 


1089 


52.13 




526 


8.54 


0.0034 


8 


Distal 


Proximal 


884 


802 


1102 


52.43 




36 


0.80 


0.3697 


9 


NIC 


Proximal 


1042 


909 


1146 


53.41 




79 


3.34 


0.0675 


10 


Total 




36313 


33769 


1075 


51.82 


230 


869 


6.36 


0.0117 


11 


Japan 


1950-55 


9973545 


9453597 


1055 


51.34 











Source: RERF TR 8-71 (Refll); 

Distal = Distally exposed (Estimated dose < 5 mSv); Proximal = Proximally exposed 10mSv+; NIC =Not in city at the 
time of the bomb 

Table 1 Sex ratio changes and the missing zygotes. Children of Hiroshima-Nagasaki by parental dose and sex 1948-53 



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ECRR Proceedings Lesvos 2009 



Table 2. Life Span Study- Persons, person years, deaths till 1972 and relative risks by cause of deaths and dose groups 



dose 


Persons 


Person- 


Observed Death 


SolidTumours 






Other Diseases 




Group 


in 1950 


Years 


till 1972 


Per 


Rela- 


Chi 


P 


Per 


Rela- 


Chi 


P 


Rad (R) 




till 1972 


Solid 


Other 


1000 


tive 


Square 




1000 


tive 


Square 










Tumor 


Diseases 


pyrs 


Risk 






pyrs 


Risk 






(b) 


(c) 


(d) 


(e) 


(f) 


(g) 


(h) 


(i) 


0) 


(k) 


(1) 


(m) 


(n) 


NICLE 


21915 


418612 


757 


3114 


1.8 








7.4 








NICEE 


4608 


85846 


210 


752 


2.4 


100 


14.8 


0.0001 


8.8 


100 


15.91 


0.00006 


OR 


34642 


685040 


1434 


5955 


2.1 


86 


10.5 


0.0010 


8.7 


99 


49.18 


0.00000 


1 -9R 


20492 


407022 


798 


3432 


2.0 


80 


2.5 


0.1100 


8.4 


96 


25.34 


0.00000 


10-49 R 


14407 


285593 


630 


2507 


2.2 


90 


13.4 


0.0002 


8.8 


100 


37.67 


0.00000 


50-99 R 


3896 


77206 


183 


693 


2.4 


97 


10.5 


0.0010 


9.0 


102 


19.69 


0.00000 


>100rads 


5676 


113294 


262 


907 


2.3 


95 


3.2 


0.0700 


8.0 


91 


3.39 


0.65 


Total 


105636 


2072613 


4274 


17360 


2.1 


84 






8.4 


96 







* Relative risks estimated using the mortality data ofNICLE; Other diseases include non-malignant diseases and leukemias. 

NIC LE = Not in city, late entrants. NIC EE = not in city early entrants. 

Source: Table 1 p 20. Table 2 p22, Table 5.1 p4 3 and Table 8.1 p64 of ABC C Life span study Technical Report No 15-73 



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ECRR Proceedings Lesvos 2009 



Somatic Effects 



In the case of mortality study, during 1950-72, there were 1,358 deaths attributable 
to radiation. In the latest LSS report for 1950-97, 440 or 8% of the total cancer 
death and 275 or less than 1% of the total non-cancer deaths was attributed to the 
bombs. This is about ten times lower than the risk estimated from our reanalysis. In 
1975 RERF stopped publication of the mortality statistics of NIC. According to 
Preston et al "this group has routinely been excluded from LSS mortality and cancer 
incidence analyses because of concerns about the comparability of their mortality 
rates to those for the rest of the cohort." 19 These concerns have not been made 
public so far. NIC is the control group is all the genetic studies of RERF. They have 
been used as the control group in recent LSS reports like the incidence of cancer in 
people exposed in childhood or in-utero 20 and in the study of incidence of cancer in 
LSS during 1958-98. Preston et al say: "in contrast to the first LSS cancer incidence 
report in 1994, the so-called NIC group was included in the new analyses because 
the addition of about 25,000 cohort members considerably improves the precision of 
the descriptions of baseline cancer risk patterns." 21 The distally exposed group had 
35,545 members (in 1950) and 918,200 person-years till 1997. The reason for 
reinventing the NIC may be more than an improvement in the precision of baseline 
risk. Incidence of cancer per 100,000 person-years in dose groups NIC, <5 mSv and 
5- 100 mSv was 587, 610, and 604 respectively. 

Nanotoxicity of fission particles 

Fission products are single atom particles with a diameter of less than one 
nanometer (nm= billionth of a meter). Nuclear weapon tests, accidents, and routine 
releases from nuclear facilities have released more than 10 30 SAPs since 1940. The 
bio-kinetics and bio-activity of particles of this size are not well known. Because of 
their high surface area to mass ratio, nanoparticles generate reactive oxygen species 
that cause DNA mutation. In other words, the fission particles have both size- 
dependent and radiological toxicity. The ICRP model for deposition of particles for 
the respiratory tract is based on studies for particles above 100 nm (0.1 |im). Fission 
products and bomb debris in the size range of nucleation mode particles (-10 nm) 
can also move up the food chain more efficiently. "Micron-sized zooplankton and 
larger filter-feeding organisms make up the basis of aquatic food webs. Many 
filtering apparatuses of filter feeders do not selectively strain items from the water; 
rather they take all nano-sized materials" 22 . The same is true for the immune system 



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ECRR Proceedings Lesvos 2009 

surveillance inside the body; the macrophages do not recognize fission products as 
foreign bodies. 

The Ethical issue of withholding data 

RERF researchers had found two serious health problems within a segment of their 
study population. The first was an abnormally high sex ratio in some of the cohorts, 
which was similar to the child sex ratio in India now, a topic that was discussed in 
the academic journals 23 and in the lay press. The second problem was the 
'inconsistent' mortality pattern of NIC cohort. These findings were ignored as they 
were immaterial for their hypothesis. Leave alone chasing the etiology of these 
serious health problems, the authors did not even bother to state what the 
inconsistency was. If NIC members were dying earlier than normal, as life time 
participants in an epidemiological study, they have a right to know why. Can 
epidemiologists ignore serious health anomalies found in their subjects because they 
are unrelated to the hypothesis? 

CONCLUSION 

Exclusion of nano-sized fission products, unfissioned plutonium and uranium, and 
neutron activation products from the dosimetry, inclusion of people exposed to these 
in the control groups, endless dis-aggregation and mismanagement of data resulted in 
underestimation health risks of the survivors. The finding of significant aberration in 
SR of NIC offspring and higher mortality risks among NIC EE and distally exposed 
cohort are unequivocal evidences for the impact of exposure to residual radiations. 
ABCC-RERF studies have almost all the features of a prospective epidemiological 
study and have large number of exposed persons of both sexes, followed up for over 
six decades. The studies that were initiated in the middle of the last century are likely 
to continue for another three-four decades. The reports of RERF, the biggest and the 
oldest environmental health research facility on earth, are considered as the final 
word by the radiation standard setting agencies and independent analysts as well. 
These studies will reveal the true genetic and somatic impacts of ionizing radiation if 
the anomalies in dosimetry are corrected. 

Acknowledgements : 

I did not receive any funding for this study. Advisory supports from Dr 

Rosalie Bertell and Dr Chris Busby are gratefully acknowledged. The data 

used in this review belong to the Radiation Effects Research Foundation, 

Hiroshima. 



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1 UNSCEAR, Exposures to the public from man-made sources of radiation 
Annex C , table 1, 2000: 197. www.unscear.org accessed on 20 Jun 2002 

2 Kudo A, Zheng J, Koerner RM et.al , Global Transport Rates of 137Cs 
and 239/240Pu Originating from the Nagasaki A-bomb in 1945 as 
Determined from Analysis of Canadian Arctic Ice Cores. 1998; J. Environ. 
Radioactivity, 40:289-298, DOI PII:S0265-93 IX (97)00023- 

3 Pace N, Smith RE. Measurement of the residual radiation intensity at the 
Hiroshima and Nagasaki atomic bomb sites. 1959; ABCC TR 26, pp 15-16. 

4 Yasuhito S. Activities at the Atomic Bomb Survivors Health Care 
Commission, Acta medica Nagasakiensia, 2005:50(supl.2), 1 1-13. 
http://naosite.lb.nagasaki-u.ac.jp. /Accessed on 23 Jan 1 1 

5 Muller HJ. Artificial transmutation in the gene, Science 1927; 66, 84-87 

6 Schull WJ, Neel JV, Hashizume A. Further observations on sex ratio 
among infants born to survivors of the atomic bombs. ABCC TR 13; 
1965. 

7 Dickinson,HO, Parker L, Binks K, Wakeford R,Smith J. The sex ratio of 
children in relation to paternal preconceptional radiation dose: a study in 
Cumbria, northern England, Jl of Epidemiology and Community Health, 
1996; 50,645-52 

8 Scherb H, Voigt K. Trends in the human sex odds at birth in Europe and the 
Chernobyl Nuclear Power Plant accident, Reproductive Toxicology; 2007; 
23 593-9. 

9 Davis DL, Gottlieb MB, Stampnitzky JR. Reduced Ratio of Male to 
Female Births in Several Industrial Countries-A Sentinel Health Indicator? 
JAMA. 1998;279(13):1018-23. doi:10.1001/jama.279.13.1018 

10 Neel JV, Schull WJ, McDonald DJ, Morton NE, Kodani M, Takeshima K et 
al. The effect of exposure to the atomic bombs on pregnancy termination in 
Hiroshima and Nagasaki : Preliminary Report. Science, 1953; 118, 537-41. 

1 1 Schull WJ, Otake M, Neel JV. A reappraisal of the genetic effects of the 
atomic bombs - Summary of a 34 year study. RERF TR 7; 1981. 

12 Schull W J, Otake M, Neel JV. Genetic Effects of Atomic bombs: A 
reappraisal, Science 1 98 1,;213: 1220-7 

13 Schull WJ, Neel JV, Hashizume A. Some Further Observations on the Sex 
Ratio Among Infants Born to Survivors of the Atomic Bombings of 
Hiroshima and Nagasaki, in Neel JV and Schull W (ed) The Children of 
Atomic Bomb Survivors: A Genetic Study 1991, National Academy Press, 
Washington, page 289, http://books.nap.edu/openbook.php , read on 30 Jan 
2011 



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ECRR Proceedings Lesvos 2009 

.14 Nakamura N. Genetic effects of radiation in Atomic bomb survivors and 

their children : Past, Present and Future, 2006; J Rad Res,47: Supple. B67- 
B73 

15 United Nations. Demographic yearbook, 17th edition (1965). 

16 Dean AG, Arner TG, Sunki GG, et al Epi Info™, Centers for Disease 
Control and Prevention, Atlanta, Georgia, USA 

17 Moriyama IM, Kato,H. Mortality Experience of A-Bomb Survivors, 1950- 
72, 1973; ABCC Technical Report 15-73 

18 OMIM Statistics for November 17, 2010, 
http://www.ncbi.nlm.nih.gov/Omim/mimstats.htmL accessed on 17 Nov 10 

19 Preston,DL, Shimizu Y, Pierce DA, Suyama A, Mabuchi K. Studies of 
Mortality of Atomic Bomb Survivors. Report 13: Solid Cancer and 
Noncancer Disease Mortality: 1950-1997, Radiation Research; 2003: 160, 
381-407. 

20 Preston DL, Cullings H, Suyama A et al. Solid Cancer Incidence in Atomic 
Bomb Survivors Exposed In Utero or as Young Children, J Natl Cancer Inst , 
2008:, 100, 428-36, http://inci.oxfordiournals.Org/content/100/6/428.full 
Accessed on 30 Dec 10 

21 Preston DL, Ron E, Tokuoka S et al, 2007, Solid Cancer Incidence among 
Atomic Bomb Survivors, 1958-1998, RERF Update Volume 18 

http ://www.rerf. ip/library/update/pdf/2007 vol 1 8 .pdf , accessed on 01 Jan 
2011 

22 Oberdorster G, Oberdorster E, Oberdorster J. Nanotoxicology: An Emerging 
Discipline Evolving from Studies of Ultrafine Particles, Environ Health 
Perspectives. 2005; 113:823-39 . doi:10.1289/ehp.7339 http:/dx.doi.org/, 
accessed 09 Feb 10 

23 Jha P, Kumar R, Vasa P, Dhingra N, Thiruchelvam D, Moineddin R, Low 
male-to-female sex ratio of children born in India: national survey of 1-1 
million households, Lancet, 2006; www.thelancet.com 
DOI:10.1016/S0140-6736(06)67930-0. Accessed on 17 Mar 08 



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19 

On the Assessment of Adverse Consequences of 

Chernobyl APS Accident on Health of Population and 

Liquidators 

E.B. Burlakova 

Emanuel Institute of Biochemical Physics, Russian Academy of Sciences, 

Moscow, 119991 Russia 

Since 1987 till the present time, at the Emanuel Institute of Biochemical Physics, 
Russian Academy of Sciences, studies on the effect of low-dose low-level 
irradiation on biophysical and biochemical parameters of the genetic and membrane 
apparatus of cells of organs of exposed animals are being carried out. 

We investigated the structural parameters of the genome (by the method of 
DNA binding to nitrocellulose filters), structural parameters of nuclear, microsomal, 
mitochondrial, and plasmic (synaptic and erythrocyte) membranes (by the method of 
spin probes localized in various layers of membranes), the composition and 
oxidation degree of membrane lipids, and the functional activity of cells - the 
activity of enzymes, relationship between isozymic forms, and regulating properties. 
We investigated also the effect of low-level irradiation on the sensitivity of cells, 
biopolymers, and animals to subsequent action of various damaging factors, 
including high-dose irradiation. The animals were exposed to a source of 137 Cs y- 
radiation at the dose-rates 41.6 x 10" 3 , 4.16 x 10" 3 , and 0.416 x 10" 3 mGy. The doses 
were varied from 6 x 10" 4 to 1.2 Gy. 

As a result of the studies performed, the following conclusions were made: 

1 . Low radiation doses affect actively the metabolism of animals and man. 

2. Over certain dose ranges, low-level irradiation is even more effective than 
acute high-level. 

3. The dose-effect dependence of irradiation may be nonlinear, nonmonotonic, 
and polymodal in character. 

4. Doses that cause the extreme effects depend on the irradiation dose-rate 
(intensity); they are lower at a lower intensity. 

5. . Low-dose irradiation causes changes (mainly, enhancement) in the 
sensitivity to the action of other damaging factors. [1,2] 



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ECRR Proceedings Lesvos 2009 

We explain the nonlinear and nonmonotonic dose-effect dependence that 
we obtained in our experiments with low-dose low-level irradiation by changes in 
the relationship between damages and reparation of the damages. With this kind of 
low-level irradiation, the reparative systems either are not initiated (induced), or 
function inadequately, or are initiated with a delay, i.e., when the exposed object has 
already received radiation damages. 

Recently, the absence of reparation at low irradiation doses was verified ont 
the cell level, [3] and the complex character of the dose dependence was confirmed 
[4]. Previously, we published a similar scheme of dependence of damages on 
irradiation dose, which was different for different dose ranges. According to the 
scheme, the quantitative characteristics were similar for the doses that differed by 
several orders of magnitude; in a certain dose range, the effect may have an opposite 
sign. 

The results obtained and supported by numerous experiments are important 
because the above dose dependences made it possible to come to conclusion about a 
radiogenic or non-radiogenic character of changes observed in an irradiated 
organism. The indisputable conclusion that if the effect increases with the dose it is 
evidence for its radiogenic nature is by no means in favor of an opposite statement, 
i.e., that the absence of a direct dose-effect dependence but its nonmonotonic 
character is evidence for the absence of a relation of the effect to irradiation. 

In autumn 2005, there were published the UNSCEAR Report and materials 
of the IAEA, WHO, and the UNDP Commission on results of analysis of the 
Chernobyl APS accident consequences including its harmful effects on health of 
population and liquidators. The data reported are in contradiction with the 
conclusions of many Russian scientists and other International organizations such as 
the American National BEIR Committee (on biological effects of Ionizing radiation) 
[5]. The controversy stems mainly from the underestimation and misunderstanding 
of the effects of low irradiation doses, reluctance to apply other criteria to assess the 
consequences, and conviction (groundless) that low doses cause either no damages 
or such minor damages that they may be neglected and disregarded. 

Neither IAEA nor WHO while defining the irradiation risks took into 
account the phenomena associated with the action of low irradiation doses and 
increase the risks; these are the programmed death of cells (apoptosis), 'bystander 
effect', and radiation-induced instability of the genome, which, in turn, results in 
enhancement of the sensitivity of organisms to the action of other damaging factors 
and more serious forms of development of diseases of other than the radiation 



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ECRR Proceedings Lesvos 2009 

genesis. The BEIR-7 reports on sources of errors made while analyzing the state of 
health of irradiated contingents of people and on the danger of low-level ionizing 
radiation for health. In the Report, the conclusion made previously that there are no 
safe levels of radiation, i.e., even very low doses may cause cancer, has been 
confirmed. 

Low-level radiation causes also other health disorders such cardiac diseases 
and insults, hepatites, mental diseases, and others. 

The factor of dose effectivenes and dose-rate for low doses was decreased 
from 2 to 1.5, which means that the anticipated amount of harmful effects of low 
doses on health is higher than it was considered earlier (see BEIR-7 Report, 2005). 

Similar recommendations for assessment of low-dose risks were made by 
Russian scientists, who published five monographs on the effects of low doses of 
radiation on health. 

We will emphasize some of the commentaries on the IAEA, WHO, and 
UNDP reports. 

1. No consideration was given to changes in the morbidity rates, which, 
according to the experts, are related to the accident as a social (not only 
radiation) risk factor, i.e., stress caused by the accident, necessity of leaving 
for other regions, changes in the living conditions, radiophobia (fear of 
radiation), etc. The IAEA and WHO disregard these diseases as a result of 
the accident. 

2. No consideration was given to those oncological diseases, for which no 
usual dose-effect dependences were determined and can be explained in 
terms of conventional models, although the radiogenic nature of diseases 
caused by low irradiation doses should be determined by using specific 
biomarkers, in accordance with requirements of molecular epidemiology, 
but not on the basis of dose dependences. 

3. No consideration was given to other somatic non-oncological diseases, 
although, according to L. Preston [6], the radiation component is an 
important one for a great number of such diseases. Ivanov et al. [7] showed 
that cerebrovascular diseases of liquidators are of the radiogenic nature. One 
should not deny the possibility of increasing these diseases as a result of the 
accident. For example, the number of radiation-induced non-cancer thyroid 
diseases of children should be taken into account while summing-up the 
results of irradiation effects on health of people. The IAEA and WHO do 
not take them into account. 



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ECRR Proceedings Lesvos 2009 

4. Neither IAEA nor WHO consider the high level of invalidity of liquidators. 
About 57% of liquidators were acknowledged invalids; for 95% of them, the 
invalidity is caused by the ChAPS accident. 

5. At present, the problem of premature aging of liquidators is under wide 
discussion; there exists a great difference between the biological and 
passport age for them. The phenomenon is not taken into account as relevant 
to deterioration of health. 

6. The IAEA and WHO consider only thyroid cancers as adverse effects on 
health of children irradiated after the Chernobyl accident. However, the 
deterioration of the children health associated with occurrence of more than 
one chronic diseases is not taken into account. The deterioration of health of 
children of liquidators is not taken into account too. 

One more source of errors in assessment of consequences of the accident is a choice 
of control groups. Usually, to determine the relation of a disease to irradiation, two 
kinds of control are used: (a) the internal control, i.e., people of the same age and 
living under the same conditions as those under study but who received considerably 
lower irradiation doses than the cohort of people under study and (b) the external 
control, for which average values are considered that were recorded for the 
population of Russia and other regions. Each of the above approaches has 
advantages and drawbacks. However, it should be noted that if a dose-effect curve 
has no threshold but is appreciably nonlinear and has an extremum point in the range 
of low doses, the choice of the internal control may lead to a false decrease in the 
relative risk of morbidity for the cohort under study and make an illusion of a 
favorable effect of irradiation. 

Note that the IAEA and WHO do not deny categorically the radiogenic 
nature of a great number of somatic diseases but do not consider them as a 
consequence of the ChAPS accident except for the statement that there is no enough 
statistical reliability of the results obtained. 

References 

1 . Burlakova E.B., Goloshchapov A.N., Zhizhina G.P., and Konradov A.A.*j; New 
aspects of effects of low doses of low-level irradiation, Radiats. Biol. 
Radioecol., 1999, vol.32, no. 1, pp. 26-34. (in Russian) 



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ECRR Proceedings Lesvos 2009 

2. Burlakova E.B., Goloshchapov A.N., Gorbunova N.V., et al., Radiats. Biol. 
Radioecol., 1996, vol. 36, no. 4, pp. 610-631. (in Russian) 

3. Rothkamm K. and Loebrich M., Evidence for a lack ofDNA double-strand 
break repair in human cells exposed to very low x-ray doses, Proc. 
Nation. Acad. Sci. USA, April 29, 2003, vol. 100, no.9, pp. 5057-5062. 

4. Hooker A.M., Bhat M., Day T.K., et al., The Linear No-Threshold Model does 
not Hold for Low-Dose Ionizing Radiation, Radiat. Res., 2004, vol. 162, 
pp.447_452. 

5. BEIR-7 Report, 2005. 

6. Preston D.L.Y, Shimizu D.A., Pierce, et al., Radiat. Res., 2003, vol. 160 (4), 
pp. 381-407. 

7. Ivanov V.K., Chekin S.Y., Parshin V.S., et al., Non-cancer thyroid diseases 
among children in the Kaluga and Bryansk regions of the Russian Federation 
exposed to radiation. 



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19 
Perinatal mortality in contaminated regions of Ukraine 
after the Chernobyl accident 

A. Korblein 1 , N. Omelyanets 2 

1 Munich Environmental Institute, Munich, Germany 
ak@umweltinstitut . org 

2 Research Centre for Radiation Medicine AMS of Ukraine, Kiev 
omelyan2006@narod.ru 

Abstract 

Perinatal mortality rates in the Ukrainian regions most affected by the Chernobyl 
fallout - Zhitomir oblast, Kiev oblast and the city of Kiev (study region) - show a 
rise and fall during the 1990's relative to the rest of Ukraine (control region). A 
biological model, which was previously applied to perinatal mortality data from 
Belarus, 1985-1998, and to perinatal mortality in Germany following the 
atmospheric nuclear weapon tests, interprets the observed increase as a late effect 
from incorporated strontium-90. The observed effect translates to 1048 excess 
perinatal deaths in the study region until 2004. 

Introduction 

In 1987 the year following the Chernobyl accident, a short-term increase of perinatal 
mortality rates was found in Germany. This increase was shown to correlate with 
incorporated radioactive caesium [1] which has a short biological half-life of only 
some months. After the atmospheric weapons tests in the 1960's, a deviation from 
the long-term trend of perinatal mortality was observed in West Germany with the 
maximum incidence in 1970, seven years after the peak fallout in 1963. This 
increase was interpreted as a late effect of incorporated strontium [2]. In the regions 
of Belarus and Ukraine near the Chernobyl site, strontium soil depositions exceeding 
1 Ci/km 2 (37 kBq/m 2 ) were detected outside the 30 km exclusion zone. A late effect 
of strontium on perinatal mortality rates could therefore be expected in the regions 
neighbouring the Chernobyl reactor. Actually, a rise of perinatal mortality rates in 
the Gomel region {oblast) relative to the rest of Belarus was found in the 1990's 
which could be associated with incorporated strontium [3]. In the present study, the 



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ECRR Proceedings Lesvos 2009 

perinatal mortality rates in the three most contaminated Ukrainian regions Zhitomir 
oblast, Kiev oblast and Kiev city are compared with the rest of Ukraine. 

Data and Methods 

All data in this study are from the State Committee of Statistics of Ukraine and the 
Ministry of Public Health of Ukraine. Ukrainian data on maternal age distribution 
(needed to calculate the average strontium burden of pregnant women) were not 
available, so Belarus data from the Statistics Department of the Ministry of Health 
of Belarus were used instead. 

Using the approach adopted in [3], the perinatal mortality rates in the two most 
contaminated Ukrainian oblasts and Kiev city are compared with the corresponding 
rates in the rest of Ukraine to ascertain possible effects of strontium in the 1990's. 
This approach has the advantage that no assumptions have to be made for the secular 
trend of the data. If the study and control regions differ in radiation contamination 
but are similar in socio-economic structure, other factors that might have a global 
influence on infant mortality in Ukraine should not influence the ratio of the 
perinatal mortality rates in the study and the control region. 
Instead of the rate ratios, the odds ratios (OR) are used which are defined by 

OR = pi/(l-pi)/(po/(l-po)) 

where pi and p are the rates in the study region (1) and the control region (0). For 

Pi, p « 1 the odds ratios approach the rate ratios. 

For the data analysis the logarithms of the odds ratios are used. A population 

weighted non-linear regression model of the form 

(1) log(OR) = p + M + P2-Sr 

is applied where parameter (3 is the intercept, Pi allows for a temporal trend of the 
odds ratios, parameters |3 2 and (3 3 estimate the effect of strontium concentration (Sr) 
in pregnant women. 

The data are weighted with weights var (ln(OR)) which are defined by 

var(ln(OR))=l/(SB 1 +NE0 1 )+l/(LB 1 -NE0 1 )+l/(SB +NEOo)+l/(LB -NEOo), 

where LB, SB and NEO are the numbers of live births, stillbirth and early neonatal 
deaths in the study (1) and the control (0) regions, respectively. 

In addition to model (1), model (2) is applied which allows for a curvilinear shape of 
the dose response relationship. 



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(2) ln(OR) = p + M + P2-Sr A p 3 

Here parameter (3 3 is the power of dose. 

The following calculation of the development of strontium concentration in pregnant 
women is based on two simple model assumptions; (a) strontium incorporation 
occurs in 1986, the year of the Chernobyl accident, and (b) strontium is incorporated 
at age 14, the age of maximum bone growth [4]. A possible adverse effect of 
strontium on the newborn will only manifest several years later, at the time of birth. 
Then the average strontium concentration in a given year following 1986 is 
proportional to the percentage of pregnant women born in 1972. This percentage 
follows from the maternal age distribution. Since Ukrainian data on the maternal age 
distribution could not obtained we used data from Belarus. The data are grouped in 5 
year strata. The shaded area in Figure 1 is the average maternal age distribution in 
Belarus for 1992-1996. To determine annual values, the data were approximated by 
the superposition of two lognormal distributions (solid line in Figure 1). 

Also the strontium excretion from the body must be taken into account. According 
to the model used in ICRP Publication 67 [5], strontium excretion contains both a 
fast and a slow component. The strontium term Sr(t), which is proportional to the 
strontium concentration, thus has the following form: 

Sr(t) = F(t-1972)-(A 1 -exp(-ln(2)-(t-1986)/T 1 )+A 2 -exp(-ln(2)-(t-1986)/T 2 )) 

where F(t-1972) is the fraction of pregnant women in year t who were born in 1972. 

Ti=2.4 years and T 2 =13.7 years are effective half-lives of strontium in the female 

body. The constants Ai, A 2 and the half-lives Ti, T 2 are determined from a 

regression of tabulated values given in [5]. A more detailed description of the model 

is given in [3]. 

The function nls() of the statistical package R is used for the data evaluation [6]. 

Results 

The trends of perinatal mortality rates, 1985-2004, in the three most contaminated 
Ukrainian regions combined, i.e. Zhitomir oblast, Kiev oblast, Kiev city (study 
region), together with the rates in the rest of Ukraine (control region), are displayed 
in Figure 2. Perinatal mortality data for Kiev city were not available before 1985, 
and the definition of stillbirth was changed after 2004, so the time span for the data 
evaluation is 1985-2004. The time variable t is calendar year minus 1980, i.e., t=0 in 
1980. 



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maternal age [years] 

Fig. 19.1: Maternal age distribution in Belarus, averaged over 1992-1996, and 
interpolation curve using two superimposed lognormal distributions 



The results of a regression of the odds ratios of perinatal mortality with a linear 
strontium term (p 3 =l) are listed in Table 1. The residual sum of squares (SSE) is 
31.4 with 17 degrees of freedom (df=17). 

Table 19.1: Regression results with model (1) 



parameter 


meaning 


estimate 


SE 


t-value 


p-value 


Po 


intercept 


0.0732 


0.0279 


2.628 


0.0176 


Pi 


temporal trend 


-0.0078 


0.0023 


-3.456 


0.0030 


h 


strontium effect 


0.0564 


0.0092 


6.124 


1.1E-05 



The odds ratios show a significant time trend (p=0.003). The strontium term is 
highly significant (p < 0.0001). 

A regression of the data using the full model (eq.l), which allows for a curvilinear 

dose response, leads to an appreciable reduction of the sum of squares (SSE=26.8, 

df=16); the F test yields p=0.119. The effect of the strontium term (parameters |3 2 

and (3 3 ) on the goodness of fit is highly significant; the sums of squares are 100.6 



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ECRR Proceedings Lesvos 2009 

(df=18) without and 26.8 (df=16) with the strontium term (F=22.0; p=3E-6; F test 
with 2 and 16 degrees of freedom). The parameter estimates are given in Table 2. 

Table 2: Regression results with model (2) 



parameter 


meaning 


estimate 


SE 


t-value 


p-value 


Po 


intercept 


0.0767 


0.0265 


2.891 


0.0106 


3. 


temporal trend 


-0.0063 


0.0023 


-2.746 


0.0144 


02 


strontium effect 


0.0196 


0.0199 


0.984 


0.3396 


03 


power of dose 


1.8031 


0.7660 


2.354 


0.0317 



The best estimate of the power of dose is 1.80 ± 0.77. Figure 3 shows the trend of 
the odds ratios and the regression line. 

Discussion 

The present study finds a highly significant association of perinatal mortality rates in 
the most contaminated regions of Ukraine (Zhitomir oblast, Kiev oblast and Kiev 
city) with the calculated strontium burden of pregnant women. The increase 
translates to 1048 excess perinatal deaths. The peak deviation from the long-term 
trend is observed in 1993, 7 years after the Chernobyl accident. There is no 
appreciable increase in 1987, the first year after the Chernobyl accident, when the 
main effect from caesium is expected. 

In West Germany, a similar deviation from the secular trend of perinatal mortality 
was found after the atmospheric nuclear weapons tests which peaked in 1970, seven 
years after the maximum fallout intensity. The same model as in the present analysis 
was applied, i.e., the excess perinatal mortality was interpreted as a late effect of 
incorporated strontium. The best estimate of the power of dose in the strontium term 
was 1.9 [2]. 

Our results contradict the negative findings reported in the WHO report published in 
2005 [7]. Inter alia, the WHO report evaluated data of pregnancy outcome from 
Ukraine and the other countries of the former Soviet Union and stated that they were 
mostly of a descriptive nature and provided only percentage changes without 
specification of the time period and the actual numbers involved. So the WHO 
Expert Group concluded that it was not able to evaluate the evidence and draw 
conclusions 



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ECRR Proceedings Lesvos 2009 



TO 10 - 
O 

E 




-study region 
-control region 



calendar years 



Fig. 19.2: Trends of perinatal mortality rates in Zhitomir oblast, Kiev oblast and 
Kiev City combined (study region) and in the rest of Ukraine (control region). 




1985 1987 1989 1991 



1993 1995 1997 

calendar years 



Fig. 19.3: Odds ratios of perinatal mortality rates in Zhitomir oblast, Kiev oblast 
and Kiev city combined (study region) and in the rest of Ukraine (control region). 
The solid line is the regression result, the broken line is the expected undisturbed 
trend of the odds ratios. 

The WHO report does not deal with perinatal mortality but it contains data on infant 
mortality. The time trends of infant mortality in the contaminated Ukrainian oblasts 
of Zhitomir and Kiev and their most highly contaminated districts (5 each) are 
compared with the corresponding rates in Poltava oblast, a so-called "clean" area. In 
Poltava oblast, the rates exhibit a monotonously falling trend during 1981-2000, but 
in the highly contaminated Zhitomir and Kiev oblasts the rates in 1991-1995 were 



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ECRR Proceedings Lesvos 2009 

higher than in 1986-1990 and in 1996-2000. The authors of the report state that no 

clear trend of infant mortality was found. 

Our results challenge the concept of a dose threshold of around 100 mGy fetal dose 

of low-LET radiation for teratogenic effects [8] since the estimated individual foetal 

doses were only in the range of some mSv in the years following the Chernobyl 

accident. 

The results of this study should be interpreted with due caution since they are based 

on highly aggregated data. But as long as there is no other feasible way to study 

small radiation effects in large human populations the findings must not be 

dismissed on grounds of the inherent limitations of the ecological study design. 

References 

1. Korblein A. Kuchenhoff H. Perinatal mortality in Germany following the 
Chernobyl accident. Radiat Environ Biophys 1997 Feb;36(l):3-7. 

2. Korblein A. Perinatal mortality in West Germany following atmospheric nuclear 
weapons tests. Arch Environ Health 2004 Nov;59(l l):604-9. 

3. Korblein A. Strontium fallout from Chernobyl and perinatal mortality in 
Ukraine and Belorussia. Radiats Biol Radioecol 2003 Mar-Apr;43(2): 197-202. 

4. Tolstykh E I. Kozheurov V P. Vyushkova O V. Degteva M O. Analysis of 
strontium metabolism in humans on the basis of the Techa river data. Radiat 
Environ Biophys 1997; 36: 25-29. 

5. International Commission on Radiological Protection (1993). Age dependent 
doses to members of the public from intake of radionuclides: Part 2: Ingestion 
dose coefficients. ICRP Publication 67, Annals of the ICRP 23, Nos. 3-4. 
Pergamon Press, Oxford. 

6. R Development Core Team (2006). R: A language and environment for 
statistical computing. R Foundation for Statistical Computing, Vienna, Austria. 
ISBN 3-900051-07-0, URL http://www.R-project.org. 

7. Health Effects of the Chernobyl Accident and Special Health Care Programmes. 
Twenty Years of Experience. Report of the UN Chernobyl Forum Expert Group 
"Health" (EGH), August 3 1 , 2005. 

8. International Commission on Radiological Protection (2003). Biological effects 
after prenatal irradiation (Embryo and Fetus). ICRP Publication 90, Annals of 
the ICRP 33, Nos. 1-2. Pergamon Press, Oxford. 

9. Environmental Consequences of the Chernobyl Accident and Their 
Remediation. Twenty Years of Experience. Report of the UN Chernobyl Forum 
Expert Group "Environment" (EGE), August 31, 2005. 



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Appendix: Perinatal mortality data in the study and control regions 





study region 


control region 


year 


live births 


stillbirths 


early 

neonatal 

deaths 


live births 


stillbirths 


early 

neonatal 

deaths 


1985 


91285 


906 


695 


580205 


6029 


3158 


1986 


90169 


792 


638 


612236 


6289 


3508 


1987 


79919 


762 


553 


601013 


5980 


3342 


1988 


89380 


824 


490 


565296 


5062 


3027 


1989 


82572 


718 


435 


525837 


4707 


2853 


1990 


75203 


668 


484 


506796 


4388 


2847 


1991 


71079 


593 


518 


488655 


4152 


2825 


1992 


66395 


555 


494 


463995 


3708 


2625 


1993 


61915 


488 


449 


433637 


3014 


2283 


1994 


58293 


451 


393 


404959 


2805 


1963 


1995 


55738 


432 


317 


381385 


2545 


2003 


1996 


53526 


400 


314 


360159 


2418 


1883 


1997 


50968 


404 


329 


340645 


2158 


1961 


1998 


47272 


308 


246 


324694 


1981 


1657 


1999 


44664 


273 


224 


299880 


1807 


1479 


2000 


45030 


235 


201 


295066 


1606 


1411 


2001 


44381 


229 


170 


287716 


1372 


1283 


2002 


47442 


238 


168 


295804 


1361 


1194 


2003 


50961 


234 


154 


306667 


1501 


1157 


2004 


55165 


260 


147 


316929 


1466 


1131 



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ECRR Proceedings Lesvos 2009 

ECRR - CERI 

European Committee on Radiation Risk 
Comite Europeenne sur le Risque de Nrradiation 

The Lesvos Declaration 

6th May 2009 

A. Whereas, the International Commission on Radiological Protection 
(ICRP) has promulgated certain risk coefficients for ionizing radiation 
exposure, 

B. Whereas, the ICRP radiation risk coefficients are used worldwide 
by federal and state governmental bodies to promulgate radiation 
protection laws and standards for exposure to workers and the 
general public from waste disposal, nuclear weapons, management of 
contaminated land and materials, naturally occurring and 
technologically enhanced radioactive materials (NORM and 
TENORM), nuclear power plant and all stages of the nuclear fuel 
cycle, compensation and rehabilitation schemes, etc, 

C. Whereas, the Chernobyl accident has provided the most important 
and indispensable opportunity to discover the yields of serious ill 
health following exposure to fission products and has demonstrated 
the inadequacy of the current ICRP risk model, especially as applied 
to foetal and early childhood exposures to radiation, 

D. Whereas, by common consent the ICRP risk model cannot validly 
be applied to post-accident exposures, nor to incorporated radioactive 
material resulting in internal exposure, 

E. Whereas, the ICRP risk model was developed before the discovery 
of the DNA structure and the discovery that certain radionuclides have 
chemical affinities for DNA, so that the concept of absorbed dose as 
used by ICRP cannot account for the effects of exposure to these 
radionuclides, 

F. Whereas, the ICRP has not taken into consideration new 
discoveries of non-targeted effects such as genomic instability and 
bystander or secondary effects with regard to understanding radiation 
risk and particularly the spectrum of consequent illnesses, 



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ECRR Proceedings Lesvos 2009 

G. Whereas, the non-cancer effects of radiation exposure may make it 
impossible to accurately determine the levels of cancer consequent 
upon exposure, because of confounding causes of death, 

H. Whereas, the ICRP considers the status of its reports to be purely 
advisory, 

I. Whereas, there is an immediate, urgent and continuing requirement 
for appropriate regulation of existing situations involving radioactivity, 
to protect the human population and the biosphere, 

We the undersigned, in our individual capacities 

1 . assert that the ICRP risk coefficients are out of date and that use of 
these coefficients leads to radiation risks being significantly 
underestimated, 

2. assert that employing the ICRP risk model to predict the health 
effects of radiation leads to errors which are at minimum 10 fold while 
we are aware of studies relating to certain types of exposure that 
suggest that the error is even greater, 

3. assert that the yield of non-cancer illnesses from radiation 
exposure, in particular damage to the cardio-vascular, immune, 
central nervous and reproductive systems, is significant but as yet 
unquantified, 

4. urge the responsible authorities, as well as all of those responsible 
for causing radiation exposures, to rely no longer upon the existing 
ICRP model in determining radiation protection standards and 
managing risks, 

5. urge the responsible authorities and all those responsible for 
causing exposures, to adopt a generally precautionary approach, and 
in the absence of another workable and sufficiently precautionary risk 
model, to apply without undue delay the provisional ECRR 2003 risk 
model, which more accurately bounds the risks reflected by current 
observations, 

6. demand immediate research into the health effects of incorporated 
radionuclides, particularly by revisiting the many historical 
epidemiological studies of exposed populations, including re- 



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ECRR Proceedings Lesvos 2009 

examination of the data from Japanese A-bomb survivors, Chernobyl 
and other affected territories and independent monitoring of 
incorporated radioactive substances in exposed populations, 

7. consider it to be a human right for individuals to know the level of 
radiation to which they are exposed, and also to be correctly informed 
as to the potential consequences of that exposure, 

8. are concerned by the escalating use of radiation for medical 
investigation and other general applications, 

9. urge significant publicly funded research into medical techniques 
which do not involve radiation exposures to patients. 

Statements contained herein reflect the opinions of the undersigned 
and are not meant to reflect the positions of any institution to which we 
are affiliated. 

Professor Yuri Bandazhevski (Belarus) 
Professor Carmel Mothershill (Canada) 
Dr Christos Matsoukas (Greece) 
Professor Chris Busby (UK) 
Professor Rosa Goncharova (Belarus) 
Professor Alexey Yablokov (Russia) 
Professor Mikhail Malko (Belarus) 
Professor Shoji Sawada (Japan) 
Professor Daniil Gluzman (Ukraine) 
Professor Angelina Nyagu (Ukraine) 
Dr Hagen Scherb (Germany) 
Professor Alexey Nesterenko (Belarus) 
Professor Inge Schmitz-Feuerhake (Germany) 
Dr Sebastian Pflugbeil (Germany) 
Professor Michel Fernex (France) 
Dr Alfred Koerblein (Germany) 
Dr Marvin Resnikoff (United States) 



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ECRR Proceedings Lesvos 2009 



Back Cover 



For those who wish to know the health consequences of the Fukushima catastrophe, 
the answers are to be found within this volume and in the radiation risk model of the 
ECRR. The data presented at the 2009 Lesvos conference of the European 
Committee on Radiation Risk show the real world effects of living in areas 
contaminated with the dispersed contents of an exploded nuclear reactor. Twenty 
five years of studies of people living on the Chernobyl contaminated territories has 
been enough to quantify in detail the cancers, the heart disease, the loss of lifespan, 
the congenital illnesses, even the changes in sex ratio, in childhood intelligence and 
in mental health that follow the exposures to radioactive contamination from fission 
products, activation products and uranium fuel particles. 

All of these are described in this volume in great detail, by the eminent scientists 
who have studied them. As Edmund Burke famously said, Those who don 't know 
history are doomed to repeat it ; but the true history of the health effects of exposure 
to the radioactive substances released by both the Chernobyl and Fukushima 
catastrophes have been covered up by the power of the nuclear lobby. And the main 
instrument that has been used for this is the radiation risk model of the International 
Commission on Radiological Protection, the ICRP. But as far as scientific evidence 
goes, the simplistic ICRP risk model is now bankrupt. It is now clear to all, except 
governments who depend upon the ICRP model to justify their support of nuclear 
energy and nuclear weapons, that the model is unsafe. With terrifying prescience, 
the matter was raised in 2009, in a videotaped meeting between the Scientific 
Secretary of the ECRR Prof. Chris Busby and the just-retired Scientific Secretary of 
the ICRP, Dr Jack Valentin. In this meeting, and presented in this volume, Valentin 
states quite unequivocally, that the ICRP model cannot be used to assess the risk 
from a major accident at a nuclear power station. It is not what it is for, he said. Yet 
this is just exactly what it is being used for 7 months after the Fukushima 
catastrophe. 

This is a political issue, an issue of democracy. It is also an issue for those 
involved, deciding whether to evacuate their children from the contaminated areas. 
Perfect political decisions require accurate information. For those decision-makers 
and members of the public who want to know what will happen to the people of 
Fukushima and wider areas of Japan, the information is here. 

The cornerstone of Science Philosophy is the Canon of Agreement, which 
states that the antecedent conditions of a phenomenon, when repeated, will produce 
the same phenomenon. Let no one doubt that the Chernobyl experiment, repeated in 
Fukushima, will cause the same result, a result reported in these proceedings in all 
its terrifying clarity. 



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